Structured Review

Santa Cruz Biotechnology bcl 2
NaN 3 induces mitochondria-mediated apoptosis through the expression of Pgc-1α-associated proteins in PC12 cells. (A) Expression levels of Pgc-1α, Nrf-1, Nrf-2, Tfam and Cox IV detected by western blot analysis. (B) Expression levels of procaspase-3, Bax, <t>Bcl-2</t> and cyt-c detected by western blot analysis. (C) Expression levels of pan-calcineurin A, CaMKII, p-CaMKII, p38 MAPK, p-p38 MAPK, Erk1/2 and p-Erk1/2 detected by western blot analysis. β-actin and GAPDH were used as the internal control. Band intensity ratios for each group are presented as mean ± standard deviation (n=3). *P
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Images

1) Product Images from "Sodium azide induces mitochondria-mediated apoptosis in PC12 cells through Pgc-1α-associated signaling pathway"

Article Title: Sodium azide induces mitochondria-mediated apoptosis in PC12 cells through Pgc-1α-associated signaling pathway

Journal: Molecular Medicine Reports

doi: 10.3892/mmr.2019.9853

NaN 3 induces mitochondria-mediated apoptosis through the expression of Pgc-1α-associated proteins in PC12 cells. (A) Expression levels of Pgc-1α, Nrf-1, Nrf-2, Tfam and Cox IV detected by western blot analysis. (B) Expression levels of procaspase-3, Bax, Bcl-2 and cyt-c detected by western blot analysis. (C) Expression levels of pan-calcineurin A, CaMKII, p-CaMKII, p38 MAPK, p-p38 MAPK, Erk1/2 and p-Erk1/2 detected by western blot analysis. β-actin and GAPDH were used as the internal control. Band intensity ratios for each group are presented as mean ± standard deviation (n=3). *P
Figure Legend Snippet: NaN 3 induces mitochondria-mediated apoptosis through the expression of Pgc-1α-associated proteins in PC12 cells. (A) Expression levels of Pgc-1α, Nrf-1, Nrf-2, Tfam and Cox IV detected by western blot analysis. (B) Expression levels of procaspase-3, Bax, Bcl-2 and cyt-c detected by western blot analysis. (C) Expression levels of pan-calcineurin A, CaMKII, p-CaMKII, p38 MAPK, p-p38 MAPK, Erk1/2 and p-Erk1/2 detected by western blot analysis. β-actin and GAPDH were used as the internal control. Band intensity ratios for each group are presented as mean ± standard deviation (n=3). *P

Techniques Used: Expressing, Pyrolysis Gas Chromatography, Western Blot, Standard Deviation

2) Product Images from "Protective Effects and Mechanisms of N-Phenethyl Caffeamide from UVA-Induced Skin Damage in Human Epidermal Keratinocytes through Nrf2/HO-1 Regulation"

Article Title: Protective Effects and Mechanisms of N-Phenethyl Caffeamide from UVA-Induced Skin Damage in Human Epidermal Keratinocytes through Nrf2/HO-1 Regulation

Journal: International Journal of Molecular Sciences

doi: 10.3390/ijms20010164

Effect of K36 on UVA-induced Bcl-2 expression in human epidermal keratinocytes. The representative image of the western blot ( a ) and the average value of the triplicate experiment ( b ); significant difference versus nonirradiated group: ###, p
Figure Legend Snippet: Effect of K36 on UVA-induced Bcl-2 expression in human epidermal keratinocytes. The representative image of the western blot ( a ) and the average value of the triplicate experiment ( b ); significant difference versus nonirradiated group: ###, p

Techniques Used: Expressing, Western Blot

3) Product Images from "Protective Effect of Hesperidin Against Sepsis-Induced Lung Injury by Inducing the Heat-Stable Protein 70 (Hsp70)/Toll-Like Receptor 4 (TLR4)/ Myeloid Differentiation Primary Response 88 (MyD88) Pathway"

Article Title: Protective Effect of Hesperidin Against Sepsis-Induced Lung Injury by Inducing the Heat-Stable Protein 70 (Hsp70)/Toll-Like Receptor 4 (TLR4)/ Myeloid Differentiation Primary Response 88 (MyD88) Pathway

Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

doi: 10.12659/MSM.912490

Effect of hesperidin on the expression of Bcl-2, caspase-3, TLR-4, and HSP70 protein in the lung tissue of CLP-induced lung injury mice. Mean ±SEM (n=6). ## p
Figure Legend Snippet: Effect of hesperidin on the expression of Bcl-2, caspase-3, TLR-4, and HSP70 protein in the lung tissue of CLP-induced lung injury mice. Mean ±SEM (n=6). ## p

Techniques Used: Expressing, Mouse Assay

4) Product Images from "Anticancer activity of bergenin against cervical cancer cells involves apoptosis, cell cycle arrest, inhibition of cell migration and the STAT3 signalling pathway"

Article Title: Anticancer activity of bergenin against cervical cancer cells involves apoptosis, cell cycle arrest, inhibition of cell migration and the STAT3 signalling pathway

Journal: Experimental and Therapeutic Medicine

doi: 10.3892/etm.2019.7380

Effect of bergenin at indicated concentrations on the expression of Bax and Bcl-2 proteins in HeLa cells as shown in the western blot. The experiments were carried out in triplicates. The values were considered significant at *P
Figure Legend Snippet: Effect of bergenin at indicated concentrations on the expression of Bax and Bcl-2 proteins in HeLa cells as shown in the western blot. The experiments were carried out in triplicates. The values were considered significant at *P

Techniques Used: Expressing, Western Blot

5) Product Images from "Early apoptosis in different models of cardiac hypertrophy induced by high renin-angiotensin system activity involves CaMKII"

Article Title: Early apoptosis in different models of cardiac hypertrophy induced by high renin-angiotensin system activity involves CaMKII

Journal: Journal of Applied Physiology

doi: 10.1152/japplphysiol.01383.2011

Cardiac apoptosis in SHR is prevented by Ena. A : representative blots and average data of the proapoptotic and antiapoptotic proteins Bax and Bcl-2, respectively, and the 17-kDa cleavage product of caspase-3 from control rats, SHR, and SHR treated with Ena. GAPDH signals were used as loading controls. The increased ratio Bax/Bcl-2, used as an apoptotic index, and caspase-3 activation in SHR, are prevented by Ena treatment. B : typical photographs of terminal deoxynucleotidyl transferase dUTP-mediated nick-end labeling (TUNEL) assay and 4′,6-diamidino-2-phenylindole dihydrochloride (DAPI) staining of control, SHR, and SHR treated with Ena. The mean values of TUNEL-positive cells normalized by total DAPI-stained nuclei in the bar graph below indicate that the increment in apoptosis in SHR is prevented by blocking RAAS axis. Values are means ± SE; n , no. of animals in each experimental group (in parentheses). * P
Figure Legend Snippet: Cardiac apoptosis in SHR is prevented by Ena. A : representative blots and average data of the proapoptotic and antiapoptotic proteins Bax and Bcl-2, respectively, and the 17-kDa cleavage product of caspase-3 from control rats, SHR, and SHR treated with Ena. GAPDH signals were used as loading controls. The increased ratio Bax/Bcl-2, used as an apoptotic index, and caspase-3 activation in SHR, are prevented by Ena treatment. B : typical photographs of terminal deoxynucleotidyl transferase dUTP-mediated nick-end labeling (TUNEL) assay and 4′,6-diamidino-2-phenylindole dihydrochloride (DAPI) staining of control, SHR, and SHR treated with Ena. The mean values of TUNEL-positive cells normalized by total DAPI-stained nuclei in the bar graph below indicate that the increment in apoptosis in SHR is prevented by blocking RAAS axis. Values are means ± SE; n , no. of animals in each experimental group (in parentheses). * P

Techniques Used: Activation Assay, End Labeling, TUNEL Assay, Staining, Blocking Assay

Mice with cardiomyocyte-delimited transgenic expression of CaMKII inhibitory peptide are protected from Iso-induced apoptosis. A : lipid peroxidation measured by TBARS indicates that Iso treatment increases oxidative stress in both AC3-C and AC3-I mice. B : representative blots from P-CaMKII and P-Thr 17 , and their respective total proteins, as an index of CaMKII activity, and average results, show that, under Iso treatment, only AC3-C mice increase phosphorylation of CaMKII and PLN at the CaMKII site. C : TUNEL and DAPI photographs of the different groups and mean (SE) values of these experiments, indicating a significant increment in TUNEL-positive cells normalized by total DAPI stained nuclei only in the AC3-C mice treated with Iso (***). D : typical blots of pro- and anti-apoptotic protein Bax, and Bcl-2, and mean (±SE) results in the bar graph below. GAPDH signals were used as loading controls. Iso treatment induced apoptosis only in AC3-C mice. * P
Figure Legend Snippet: Mice with cardiomyocyte-delimited transgenic expression of CaMKII inhibitory peptide are protected from Iso-induced apoptosis. A : lipid peroxidation measured by TBARS indicates that Iso treatment increases oxidative stress in both AC3-C and AC3-I mice. B : representative blots from P-CaMKII and P-Thr 17 , and their respective total proteins, as an index of CaMKII activity, and average results, show that, under Iso treatment, only AC3-C mice increase phosphorylation of CaMKII and PLN at the CaMKII site. C : TUNEL and DAPI photographs of the different groups and mean (SE) values of these experiments, indicating a significant increment in TUNEL-positive cells normalized by total DAPI stained nuclei only in the AC3-C mice treated with Iso (***). D : typical blots of pro- and anti-apoptotic protein Bax, and Bcl-2, and mean (±SE) results in the bar graph below. GAPDH signals were used as loading controls. Iso treatment induced apoptosis only in AC3-C mice. * P

Techniques Used: Mouse Assay, Transgenic Assay, Expressing, Activity Assay, TUNEL Assay, Staining

6) Product Images from "Toll-like receptor 3 plays a role in myocardial infarction and ischemia/reperfusion injury"

Article Title: Toll-like receptor 3 plays a role in myocardial infarction and ischemia/reperfusion injury

Journal: Biochimica et biophysica acta

doi: 10.1016/j.bbadis.2013.10.006

TLR3 deficiency attenuates I/R-increased FasL, Fas, FADD, Bak, and Bax expression, and prevents I/R-induced decreases in myocardial Bcl-2 levels TLR3 −/− and WT mice were subjected to myocardial ischemia (45 min) followed by reperfusion (24 h). Sham surgical operation serve as sham control. TLR3 deficiency attenuates I/R-increased the levels of Fas ( A ), FasL ( B ), FADD ( C ), Bak ( D ), and Bax (E) in the myocardium. ( F ) TLR3 deficiency increases the levels of Bcl2 in the myocardium following myocardial I/R. There were 6 mice in each group. * p
Figure Legend Snippet: TLR3 deficiency attenuates I/R-increased FasL, Fas, FADD, Bak, and Bax expression, and prevents I/R-induced decreases in myocardial Bcl-2 levels TLR3 −/− and WT mice were subjected to myocardial ischemia (45 min) followed by reperfusion (24 h). Sham surgical operation serve as sham control. TLR3 deficiency attenuates I/R-increased the levels of Fas ( A ), FasL ( B ), FADD ( C ), Bak ( D ), and Bax (E) in the myocardium. ( F ) TLR3 deficiency increases the levels of Bcl2 in the myocardium following myocardial I/R. There were 6 mice in each group. * p

Techniques Used: Expressing, Mouse Assay

7) Product Images from "Histone deacetylases mediate the silencing of miR-15a, miR-16, and miR-29b in chronic lymphocytic leukemia"

Article Title: Histone deacetylases mediate the silencing of miR-15a, miR-16, and miR-29b in chronic lymphocytic leukemia

Journal: Blood

doi: 10.1182/blood-2011-05-351510

Action of 10nM LBH589 on Mcl-1, Bcl-2, mitochondrial membrane depolarization and apotosis in CLL cells. Change in Mcl-1 (A), Bcl-2 (B), and mitochondrial membrane depolarization as measured by loss of the mitochondrial dye TMRM (C) and increase in annexin V/propidium iodide positivity after exposure to 10nM LBH589 for 48 hours (D). (E) Influence of pre-exposure to z-vad-fmk on the action of 10nM LBH589 for 48 hours on Mcl-1, appearance of cleaved caspase-3, and apoptosis in primary CLL cells (n = 4).
Figure Legend Snippet: Action of 10nM LBH589 on Mcl-1, Bcl-2, mitochondrial membrane depolarization and apotosis in CLL cells. Change in Mcl-1 (A), Bcl-2 (B), and mitochondrial membrane depolarization as measured by loss of the mitochondrial dye TMRM (C) and increase in annexin V/propidium iodide positivity after exposure to 10nM LBH589 for 48 hours (D). (E) Influence of pre-exposure to z-vad-fmk on the action of 10nM LBH589 for 48 hours on Mcl-1, appearance of cleaved caspase-3, and apoptosis in primary CLL cells (n = 4).

Techniques Used:

miR-15a and miR-16 target Mcl1 but not Bcl-2 in primary CLL cells. (A) Expression of miR-15a and miR-16 in a CLL sample after nucleofection for 48 hours. (B) Levels of Mcl-1 and Bcl-2 in a CLL sample after nucleofection with miR-15a, miR-16, or a scrambled nontargeting control (Scr) miR for 48 hours. (C) Quantitation of the levels of Mcl-1 and Bcl-2 in 10 primary CLL samples after nucleofection with miR-15a, miR-16, or a Scr miR for 48 hours. Statistical significance of the decrease of Mcl-1 and Bcl-2 levels was determined by 1-way ANOVA.
Figure Legend Snippet: miR-15a and miR-16 target Mcl1 but not Bcl-2 in primary CLL cells. (A) Expression of miR-15a and miR-16 in a CLL sample after nucleofection for 48 hours. (B) Levels of Mcl-1 and Bcl-2 in a CLL sample after nucleofection with miR-15a, miR-16, or a scrambled nontargeting control (Scr) miR for 48 hours. (C) Quantitation of the levels of Mcl-1 and Bcl-2 in 10 primary CLL samples after nucleofection with miR-15a, miR-16, or a Scr miR for 48 hours. Statistical significance of the decrease of Mcl-1 and Bcl-2 levels was determined by 1-way ANOVA.

Techniques Used: Expressing, Quantitation Assay

Relation between induction of miR-15a, miR-16, miR-29b, and decrease of Mcl-1 and Bcl-2 in response to 10nM LBH589 in CLL cells. (A) Levels of Mcl-1, Bcl-2, GAPDH, and cleaved caspase-3 at 3, 6, 18, or 24 hours in 3 CLL samples that activated miR-15a, miR-16, or miR-29b in response to 10nM LBH589. (B) Quantitation of Mcl-1 levels at various times (up to 48 hours) in 9 CLL samples that activated miR-15a, miR-16, or miR-29b in response to 10nM LBH589. (C) Quantitation of Bcl-2 levels at various times (up to 48 hours) in 9 CLL samples that activated miR-15a, miR-16, or miR-29b in response to 10nM LBH589. (D) Levels of Mcl-1, Bcl-2, GAPDH, and cleaved caspase-3 at 3, 6, 18, or 24 hours in 3 CLL samples that did not activate miR-15a, miR-16, or miR-29b in response to 10nM LBH589. (E) Quantitation of Mcl-1 levels at various times (up to 48 hours) in 11 CLL samples that did not activate miR-15a, miR-16, or miR-29b in response to 10nM LBH589. (F) Quantitation of Bcl-2 levels at various times (up to 48 hours) in 11 CLL samples that did not activate miR-15a, miR-16, or miR-29b in response to 10nM LBH589.
Figure Legend Snippet: Relation between induction of miR-15a, miR-16, miR-29b, and decrease of Mcl-1 and Bcl-2 in response to 10nM LBH589 in CLL cells. (A) Levels of Mcl-1, Bcl-2, GAPDH, and cleaved caspase-3 at 3, 6, 18, or 24 hours in 3 CLL samples that activated miR-15a, miR-16, or miR-29b in response to 10nM LBH589. (B) Quantitation of Mcl-1 levels at various times (up to 48 hours) in 9 CLL samples that activated miR-15a, miR-16, or miR-29b in response to 10nM LBH589. (C) Quantitation of Bcl-2 levels at various times (up to 48 hours) in 9 CLL samples that activated miR-15a, miR-16, or miR-29b in response to 10nM LBH589. (D) Levels of Mcl-1, Bcl-2, GAPDH, and cleaved caspase-3 at 3, 6, 18, or 24 hours in 3 CLL samples that did not activate miR-15a, miR-16, or miR-29b in response to 10nM LBH589. (E) Quantitation of Mcl-1 levels at various times (up to 48 hours) in 11 CLL samples that did not activate miR-15a, miR-16, or miR-29b in response to 10nM LBH589. (F) Quantitation of Bcl-2 levels at various times (up to 48 hours) in 11 CLL samples that did not activate miR-15a, miR-16, or miR-29b in response to 10nM LBH589.

Techniques Used: Quantitation Assay

8) Product Images from "VX680 suppresses the growth of HepG2 cells and enhances the chemosensitivity to cisplatin"

Article Title: VX680 suppresses the growth of HepG2 cells and enhances the chemosensitivity to cisplatin

Journal: Oncology Letters

doi: 10.3892/ol.2013.1648

(A) Hepatocellular carcinoma (HepG2) cells were cultured with varying concentrations of VX680 (25 and 50 μmol/l) for 24 h. All cells were collected and analyzed by western blot analysis with an anti-Aurora A antibody. (B) HepG2 cells were treated with 3.125 μmol/l VX680, 0.5 μg/ml cisplatin or a combination of the two for 72 h. Cell lysates were collected and analyzed by western blot analysis with anti-p53, anti-Bcl-2 and anti-β-actin antibodies. The protein level for each group was compared with that of the control group.
Figure Legend Snippet: (A) Hepatocellular carcinoma (HepG2) cells were cultured with varying concentrations of VX680 (25 and 50 μmol/l) for 24 h. All cells were collected and analyzed by western blot analysis with an anti-Aurora A antibody. (B) HepG2 cells were treated with 3.125 μmol/l VX680, 0.5 μg/ml cisplatin or a combination of the two for 72 h. Cell lysates were collected and analyzed by western blot analysis with anti-p53, anti-Bcl-2 and anti-β-actin antibodies. The protein level for each group was compared with that of the control group.

Techniques Used: Cell Culture, Western Blot

9) Product Images from "Autophagy and apoptosis-related genes in chronic liver disease and hepatocellular carcinoma"

Article Title: Autophagy and apoptosis-related genes in chronic liver disease and hepatocellular carcinoma

Journal: BMC Gastroenterology

doi: 10.1186/1471-230X-12-118

Schematic representation of the interplay between pro- and anti-apoptotic Bcl-2 family members and Beclin 1, in the endoplasmic reticulum and mitochondria.
Figure Legend Snippet: Schematic representation of the interplay between pro- and anti-apoptotic Bcl-2 family members and Beclin 1, in the endoplasmic reticulum and mitochondria.

Techniques Used:

mRNA analysis by quantitative absolute Real-Time PCR using SYBR Green I. Gene analysis of Beclin 1 ( A ), Bcl-2 ( B ), Bcl-xL ( C ), Bad ( D ) and Bax ( E ). Control: control specimens; CH: chronic hepatitis; CIRR: cirrhosis; PHCC: cirrhotic tissues surrounding hepatocellular carcinoma; HCC: hepatocellular carcinoma. Data are expressed as mean ± SD of the ratio of the gene of interest to that of β-actin.
Figure Legend Snippet: mRNA analysis by quantitative absolute Real-Time PCR using SYBR Green I. Gene analysis of Beclin 1 ( A ), Bcl-2 ( B ), Bcl-xL ( C ), Bad ( D ) and Bax ( E ). Control: control specimens; CH: chronic hepatitis; CIRR: cirrhosis; PHCC: cirrhotic tissues surrounding hepatocellular carcinoma; HCC: hepatocellular carcinoma. Data are expressed as mean ± SD of the ratio of the gene of interest to that of β-actin.

Techniques Used: Real-time Polymerase Chain Reaction, SYBR Green Assay

Protein expression in HCC and the corresponding tissues surrounding HCC. Western blot analysis of: Beclin 1 (A) ; Bcl-2 (B) ; Bcl-xL (C) ; Bad (D) ; Bax (E) . P: cirrhotic liver tissues surrounding hepatocellular carcinoma; HCC: tumoral tissues of 8/13 patients. Data are expressed as the optical density ratio of genes to β-actin. Values are reported as mean values ± SD.
Figure Legend Snippet: Protein expression in HCC and the corresponding tissues surrounding HCC. Western blot analysis of: Beclin 1 (A) ; Bcl-2 (B) ; Bcl-xL (C) ; Bad (D) ; Bax (E) . P: cirrhotic liver tissues surrounding hepatocellular carcinoma; HCC: tumoral tissues of 8/13 patients. Data are expressed as the optical density ratio of genes to β-actin. Values are reported as mean values ± SD.

Techniques Used: Expressing, Western Blot

10) Product Images from "Heme Oxygenase-1 Prevents Cardiac Dysfunction in Streptozotocin-Diabetic Mice by Reducing Inflammation, Oxidative Stress, Apoptosis and Enhancing Autophagy"

Article Title: Heme Oxygenase-1 Prevents Cardiac Dysfunction in Streptozotocin-Diabetic Mice by Reducing Inflammation, Oxidative Stress, Apoptosis and Enhancing Autophagy

Journal: PLoS ONE

doi: 10.1371/journal.pone.0075927

Anti-apoptotic effects of HO-1 on cardiomyocytes in diabetic mice. A. Apoptosis assessed by TUNEL assay in the respective groups (left) with quantification on the right. First column: Nuclei of apoptotic cells TUNEL stained in green. Second column: The DAPI-stained nuclei appear in blue. Third column: merged picture of first and second column (scale bar, 20µm). B. Representative immunoblot for p53 and Bcl-2 in the myocardial tissues from the respective groups (left) and densitometric quantification (right). C. Flow cytometric analysis using Annexin V-FITC and propidium iodide stains to evaluate the effects of transfection with HO-1 or empty vector (PC) under control and high-glucose culture conditions (left) with quantification on the right. D. Representative immunoblot for p-Akt, Akt, p-GSK3 and GSK3 in the myocardial tissues from the respective groups (left) and densitometric quantification (right). (n = 5 in each group) Columns and errors bars represent mean ± SD. #p
Figure Legend Snippet: Anti-apoptotic effects of HO-1 on cardiomyocytes in diabetic mice. A. Apoptosis assessed by TUNEL assay in the respective groups (left) with quantification on the right. First column: Nuclei of apoptotic cells TUNEL stained in green. Second column: The DAPI-stained nuclei appear in blue. Third column: merged picture of first and second column (scale bar, 20µm). B. Representative immunoblot for p53 and Bcl-2 in the myocardial tissues from the respective groups (left) and densitometric quantification (right). C. Flow cytometric analysis using Annexin V-FITC and propidium iodide stains to evaluate the effects of transfection with HO-1 or empty vector (PC) under control and high-glucose culture conditions (left) with quantification on the right. D. Representative immunoblot for p-Akt, Akt, p-GSK3 and GSK3 in the myocardial tissues from the respective groups (left) and densitometric quantification (right). (n = 5 in each group) Columns and errors bars represent mean ± SD. #p

Techniques Used: Mouse Assay, TUNEL Assay, Staining, Flow Cytometry, Transfection, Plasmid Preparation

11) Product Images from "Protective effects of total flavonoids from Flos Puerariae on retinal neuronal damage in diabetic mice"

Article Title: Protective effects of total flavonoids from Flos Puerariae on retinal neuronal damage in diabetic mice

Journal: Molecular Vision

doi:

Effect of total flavonoids from Flos Puerariae (TFF) on Bax and Bcl-2 expression in retinas of the diabetic mice. A : The photomicrographs were representatives the retina sections immunohistochemistry stained with Bax and Bcl-2 antibody. n=4 per group. (Magnification: 400×). Bax and Bcl-2 expression were localized in the cytosol of cells mainly in ganglion cell layer (GCL) and inner nuclear layer (INL). B : The photographs were representatives the western blot of Bax and Bcl-2 protein. Five western blots per group were experimented. C : Relative intensities of Bax protein (fold to β-actin). D : Relative intensities of Bcl-2 protein (fold to β-actin). E : Ratio of the relative intensities of Bcl-2 to Bax (Bcl-2 / Bax). Data are expressed as mean ±standard deviation. *p
Figure Legend Snippet: Effect of total flavonoids from Flos Puerariae (TFF) on Bax and Bcl-2 expression in retinas of the diabetic mice. A : The photomicrographs were representatives the retina sections immunohistochemistry stained with Bax and Bcl-2 antibody. n=4 per group. (Magnification: 400×). Bax and Bcl-2 expression were localized in the cytosol of cells mainly in ganglion cell layer (GCL) and inner nuclear layer (INL). B : The photographs were representatives the western blot of Bax and Bcl-2 protein. Five western blots per group were experimented. C : Relative intensities of Bax protein (fold to β-actin). D : Relative intensities of Bcl-2 protein (fold to β-actin). E : Ratio of the relative intensities of Bcl-2 to Bax (Bcl-2 / Bax). Data are expressed as mean ±standard deviation. *p

Techniques Used: Expressing, Mouse Assay, Immunohistochemistry, Staining, Western Blot, Standard Deviation

12) Product Images from "Type II cGMP-dependent protein kinase inhibits epidermal growth factor-induced phosphatidylinositol-3-kinase/Akt signal transduction in gastric cancer cells"

Article Title: Type II cGMP-dependent protein kinase inhibits epidermal growth factor-induced phosphatidylinositol-3-kinase/Akt signal transduction in gastric cancer cells

Journal: Oncology Letters

doi: 10.3892/ol.2013.1630

PKG II inhibits EGF-induced expression of Bcl-2. The AGS cells were treated as in Fig. 5 and harvested and lysed as described in Materials and methods. The cell lysate was subjected to western blotting with an anti Bcl-2 antibody. The results revealed that in the EGF-treated cells, the expression of Bcl-2 increased, and a higher expression and activity of PKG II prevented the EGF-induced increase of Bcl-2 expression. PKG II, cGMP-dependent protein kinase Type II; EGF, epidermal growth factor.
Figure Legend Snippet: PKG II inhibits EGF-induced expression of Bcl-2. The AGS cells were treated as in Fig. 5 and harvested and lysed as described in Materials and methods. The cell lysate was subjected to western blotting with an anti Bcl-2 antibody. The results revealed that in the EGF-treated cells, the expression of Bcl-2 increased, and a higher expression and activity of PKG II prevented the EGF-induced increase of Bcl-2 expression. PKG II, cGMP-dependent protein kinase Type II; EGF, epidermal growth factor.

Techniques Used: Expressing, Western Blot, Activity Assay

13) Product Images from "Overexpression of p65 attenuates celecoxib-induced cell death in MDA-MB-231 human breast cancer cell line"

Article Title: Overexpression of p65 attenuates celecoxib-induced cell death in MDA-MB-231 human breast cancer cell line

Journal: Cancer Cell International

doi: 10.1186/1475-2867-13-14

Effect of p65 overexpression on anti-apoptotic NF-κB target genes including Bcl-2 family and IAP family proteins.
Figure Legend Snippet: Effect of p65 overexpression on anti-apoptotic NF-κB target genes including Bcl-2 family and IAP family proteins.

Techniques Used: Over Expression

14) Product Images from "Puerarin Suppress Apoptosis of Human Osteoblasts via ERK Signaling Pathway"

Article Title: Puerarin Suppress Apoptosis of Human Osteoblasts via ERK Signaling Pathway

Journal: International Journal of Endocrinology

doi: 10.1155/2013/786574

Effects of puerarin on the expression of Bcl-2 and Bax in hOBs. Cells were treated with 0, 10 −9 M, 10 −8 M, and 10 −7 M puerarin for 48 h before collecting proteins. Cell lysates were subjected to western blot analysis and incubated with anti-Bax, anti-Bcl-2, or anti- β -actin monoclonal antibodies. Gel-Pro 4.0 gel image analysis software was used to analyze the absorbance values of Bcl-2 and Bax.
Figure Legend Snippet: Effects of puerarin on the expression of Bcl-2 and Bax in hOBs. Cells were treated with 0, 10 −9 M, 10 −8 M, and 10 −7 M puerarin for 48 h before collecting proteins. Cell lysates were subjected to western blot analysis and incubated with anti-Bax, anti-Bcl-2, or anti- β -actin monoclonal antibodies. Gel-Pro 4.0 gel image analysis software was used to analyze the absorbance values of Bcl-2 and Bax.

Techniques Used: Expressing, Western Blot, Incubation, Software

15) Product Images from "IL-17-mediated Bcl-2 expression regulates survival of fibroblast-like synoviocytes in rheumatoid arthritis through STAT3 activation"

Article Title: IL-17-mediated Bcl-2 expression regulates survival of fibroblast-like synoviocytes in rheumatoid arthritis through STAT3 activation

Journal: Arthritis Research & Therapy

doi: 10.1186/ar4179

Interleukin (IL)-17 upregulates the expression of Bcl-2 in synoviocytes in rheumatoid arthritis (RA) . ( A ) Fibroblast-like synoviocytes from patients with RA (RA-FLSs) ( n = 3) and fibroblast-like synoviocytes from patients with osteoarthritis (OA-FLSs) ( n = 3) were cultured with IL-17 (0, 1 and 10 ng/ml) for 12 hours. The mRNA expression of Bcl-2 and Bax was evaluated by real-time PCR. The Bcl-2/Bax ratio is shown in the right panel. * P
Figure Legend Snippet: Interleukin (IL)-17 upregulates the expression of Bcl-2 in synoviocytes in rheumatoid arthritis (RA) . ( A ) Fibroblast-like synoviocytes from patients with RA (RA-FLSs) ( n = 3) and fibroblast-like synoviocytes from patients with osteoarthritis (OA-FLSs) ( n = 3) were cultured with IL-17 (0, 1 and 10 ng/ml) for 12 hours. The mRNA expression of Bcl-2 and Bax was evaluated by real-time PCR. The Bcl-2/Bax ratio is shown in the right panel. * P

Techniques Used: Expressing, Cell Culture, Real-time Polymerase Chain Reaction

Bcl-2 and Bax expression in synoviocytes in rheumatoid arthritis (RA) . ( A ) Fibroblast-like synoviocytes (FLSs) from RA patients ( n = 3) and osteoarthritis (OA) patients ( n = 3) were cultured. The expression of Bcl-2 and Bax mRNA in synoviocytes was evaluated by real-time PCR. * P
Figure Legend Snippet: Bcl-2 and Bax expression in synoviocytes in rheumatoid arthritis (RA) . ( A ) Fibroblast-like synoviocytes (FLSs) from RA patients ( n = 3) and osteoarthritis (OA) patients ( n = 3) were cultured. The expression of Bcl-2 and Bax mRNA in synoviocytes was evaluated by real-time PCR. * P

Techniques Used: Expressing, Cell Culture, Real-time Polymerase Chain Reaction

Signal tranducer and activator of transcription 3 ( STAT3) mediates IL-17-induced Bcl-2 upregulation in synoviocytes in rheumatoid arthritis (RA) . ( A ) IL-17 upregulated the expression of STAT3 in RA-fibroblast-like synoviocytes (FLSs). RA-FLSs ( n = 3) were cultured with IL-17 (0, 1 and 10 ng/ml) for 12 hours. The expressions of STAT3 and phosphorylated STAT3 (pSTAT3 705 and pSTAT3 727) were measured by western blot. The representative figure is shown in the left panel. Data are expressed as mean ± SD of three independent experiments. * P
Figure Legend Snippet: Signal tranducer and activator of transcription 3 ( STAT3) mediates IL-17-induced Bcl-2 upregulation in synoviocytes in rheumatoid arthritis (RA) . ( A ) IL-17 upregulated the expression of STAT3 in RA-fibroblast-like synoviocytes (FLSs). RA-FLSs ( n = 3) were cultured with IL-17 (0, 1 and 10 ng/ml) for 12 hours. The expressions of STAT3 and phosphorylated STAT3 (pSTAT3 705 and pSTAT3 727) were measured by western blot. The representative figure is shown in the left panel. Data are expressed as mean ± SD of three independent experiments. * P

Techniques Used: Expressing, Cell Culture, Western Blot

16) Product Images from "IL-17-mediated Bcl-2 expression regulates survival of fibroblast-like synoviocytes in rheumatoid arthritis through STAT3 activation"

Article Title: IL-17-mediated Bcl-2 expression regulates survival of fibroblast-like synoviocytes in rheumatoid arthritis through STAT3 activation

Journal: Arthritis Research & Therapy

doi: 10.1186/ar4179

Interleukin (IL)-17 upregulates the expression of Bcl-2 in synoviocytes in rheumatoid arthritis (RA) . ( A ) Fibroblast-like synoviocytes from patients with RA (RA-FLSs) ( n = 3) and fibroblast-like synoviocytes from patients with osteoarthritis (OA-FLSs) ( n = 3) were cultured with IL-17 (0, 1 and 10 ng/ml) for 12 hours. The mRNA expression of Bcl-2 and Bax was evaluated by real-time PCR. The Bcl-2/Bax ratio is shown in the right panel. * P
Figure Legend Snippet: Interleukin (IL)-17 upregulates the expression of Bcl-2 in synoviocytes in rheumatoid arthritis (RA) . ( A ) Fibroblast-like synoviocytes from patients with RA (RA-FLSs) ( n = 3) and fibroblast-like synoviocytes from patients with osteoarthritis (OA-FLSs) ( n = 3) were cultured with IL-17 (0, 1 and 10 ng/ml) for 12 hours. The mRNA expression of Bcl-2 and Bax was evaluated by real-time PCR. The Bcl-2/Bax ratio is shown in the right panel. * P

Techniques Used: Expressing, Cell Culture, Real-time Polymerase Chain Reaction

Bcl-2 and Bax expression in synoviocytes in rheumatoid arthritis (RA) . ( A ) Fibroblast-like synoviocytes (FLSs) from RA patients ( n = 3) and osteoarthritis (OA) patients ( n = 3) were cultured. The expression of Bcl-2 and Bax mRNA in synoviocytes was evaluated by real-time PCR. * P
Figure Legend Snippet: Bcl-2 and Bax expression in synoviocytes in rheumatoid arthritis (RA) . ( A ) Fibroblast-like synoviocytes (FLSs) from RA patients ( n = 3) and osteoarthritis (OA) patients ( n = 3) were cultured. The expression of Bcl-2 and Bax mRNA in synoviocytes was evaluated by real-time PCR. * P

Techniques Used: Expressing, Cell Culture, Real-time Polymerase Chain Reaction

Signal tranducer and activator of transcription 3 ( STAT3) mediates IL-17-induced Bcl-2 upregulation in synoviocytes in rheumatoid arthritis (RA) . ( A ) IL-17 upregulated the expression of STAT3 in RA-fibroblast-like synoviocytes (FLSs). RA-FLSs ( n = 3) were cultured with IL-17 (0, 1 and 10 ng/ml) for 12 hours. The expressions of STAT3 and phosphorylated STAT3 (pSTAT3 705 and pSTAT3 727) were measured by western blot. The representative figure is shown in the left panel. Data are expressed as mean ± SD of three independent experiments. * P
Figure Legend Snippet: Signal tranducer and activator of transcription 3 ( STAT3) mediates IL-17-induced Bcl-2 upregulation in synoviocytes in rheumatoid arthritis (RA) . ( A ) IL-17 upregulated the expression of STAT3 in RA-fibroblast-like synoviocytes (FLSs). RA-FLSs ( n = 3) were cultured with IL-17 (0, 1 and 10 ng/ml) for 12 hours. The expressions of STAT3 and phosphorylated STAT3 (pSTAT3 705 and pSTAT3 727) were measured by western blot. The representative figure is shown in the left panel. Data are expressed as mean ± SD of three independent experiments. * P

Techniques Used: Expressing, Cell Culture, Western Blot

17) Product Images from "IL-17-mediated Bcl-2 expression regulates survival of fibroblast-like synoviocytes in rheumatoid arthritis through STAT3 activation"

Article Title: IL-17-mediated Bcl-2 expression regulates survival of fibroblast-like synoviocytes in rheumatoid arthritis through STAT3 activation

Journal: Arthritis Research & Therapy

doi: 10.1186/ar4179

Interleukin (IL)-17 upregulates the expression of Bcl-2 in synoviocytes in rheumatoid arthritis (RA) . ( A ) Fibroblast-like synoviocytes from patients with RA (RA-FLSs) ( n = 3) and fibroblast-like synoviocytes from patients with osteoarthritis (OA-FLSs) ( n = 3) were cultured with IL-17 (0, 1 and 10 ng/ml) for 12 hours. The mRNA expression of Bcl-2 and Bax was evaluated by real-time PCR. The Bcl-2/Bax ratio is shown in the right panel. * P
Figure Legend Snippet: Interleukin (IL)-17 upregulates the expression of Bcl-2 in synoviocytes in rheumatoid arthritis (RA) . ( A ) Fibroblast-like synoviocytes from patients with RA (RA-FLSs) ( n = 3) and fibroblast-like synoviocytes from patients with osteoarthritis (OA-FLSs) ( n = 3) were cultured with IL-17 (0, 1 and 10 ng/ml) for 12 hours. The mRNA expression of Bcl-2 and Bax was evaluated by real-time PCR. The Bcl-2/Bax ratio is shown in the right panel. * P

Techniques Used: Expressing, Cell Culture, Real-time Polymerase Chain Reaction

Bcl-2 and Bax expression in synoviocytes in rheumatoid arthritis (RA) . ( A ) Fibroblast-like synoviocytes (FLSs) from RA patients ( n = 3) and osteoarthritis (OA) patients ( n = 3) were cultured. The expression of Bcl-2 and Bax mRNA in synoviocytes was evaluated by real-time PCR. * P
Figure Legend Snippet: Bcl-2 and Bax expression in synoviocytes in rheumatoid arthritis (RA) . ( A ) Fibroblast-like synoviocytes (FLSs) from RA patients ( n = 3) and osteoarthritis (OA) patients ( n = 3) were cultured. The expression of Bcl-2 and Bax mRNA in synoviocytes was evaluated by real-time PCR. * P

Techniques Used: Expressing, Cell Culture, Real-time Polymerase Chain Reaction

Signal tranducer and activator of transcription 3 ( STAT3) mediates IL-17-induced Bcl-2 upregulation in synoviocytes in rheumatoid arthritis (RA) . ( A ) IL-17 upregulated the expression of STAT3 in RA-fibroblast-like synoviocytes (FLSs). RA-FLSs ( n = 3) were cultured with IL-17 (0, 1 and 10 ng/ml) for 12 hours. The expressions of STAT3 and phosphorylated STAT3 (pSTAT3 705 and pSTAT3 727) were measured by western blot. The representative figure is shown in the left panel. Data are expressed as mean ± SD of three independent experiments. * P
Figure Legend Snippet: Signal tranducer and activator of transcription 3 ( STAT3) mediates IL-17-induced Bcl-2 upregulation in synoviocytes in rheumatoid arthritis (RA) . ( A ) IL-17 upregulated the expression of STAT3 in RA-fibroblast-like synoviocytes (FLSs). RA-FLSs ( n = 3) were cultured with IL-17 (0, 1 and 10 ng/ml) for 12 hours. The expressions of STAT3 and phosphorylated STAT3 (pSTAT3 705 and pSTAT3 727) were measured by western blot. The representative figure is shown in the left panel. Data are expressed as mean ± SD of three independent experiments. * P

Techniques Used: Expressing, Cell Culture, Western Blot

18) Product Images from "Damnacanthal is a potent inducer of apoptosis with anticancer activity by stimulating p53 and p21 genes in MCF-7 breast cancer cells"

Article Title: Damnacanthal is a potent inducer of apoptosis with anticancer activity by stimulating p53 and p21 genes in MCF-7 breast cancer cells

Journal: Oncology Letters

doi: 10.3892/ol.2014.1898

Flow cytometry analysis of MCF-7 cells treated with and without damnacanthal for 72 h were analyzed for the expression of Bcl-2, estrogen receptor-α, p53 and X-linked inhibitor of apoptosis proteins. The control cells were treated with vehicle in RPMI medium. Results are representative of three independent experiments. Data are presented as the means ± standard deviation of the percentage of protein expression from four independent experiments. ** P
Figure Legend Snippet: Flow cytometry analysis of MCF-7 cells treated with and without damnacanthal for 72 h were analyzed for the expression of Bcl-2, estrogen receptor-α, p53 and X-linked inhibitor of apoptosis proteins. The control cells were treated with vehicle in RPMI medium. Results are representative of three independent experiments. Data are presented as the means ± standard deviation of the percentage of protein expression from four independent experiments. ** P

Techniques Used: Flow Cytometry, Cytometry, Expressing, Standard Deviation

19) Product Images from "RANKL increases the level of Mcl-1 in osteoclasts and reduces bisphosphonate-induced osteoclast apoptosis in vitro"

Article Title: RANKL increases the level of Mcl-1 in osteoclasts and reduces bisphosphonate-induced osteoclast apoptosis in vitro

Journal: Arthritis Research & Therapy

doi: 10.1186/ar2681

RANKL prevents activation of caspase-9 and increases Mcl-1 in osteoclasts but does not prevent inhibition of protein prenylation. Cultures of mature osteoclasts from rabbit bones were treated with 100 μM ALN ± 100 ng/mL RANKL for 48 hours and stained using an Apofluor Green Caspase-9 Activity Assay kit and Hoechst 33342. (a) A representative non-apoptotic and apoptotic osteoclast. (b) Quantification of caspase-9-positive osteoclasts after treatment with alendronate ± RANKL for 48 hours. * P ≤ 0.05 compared with ALN alone or # P ≤ 0.05 compared with control (CTL) (analysis of variance). Values are the mean ± standard error of the mean (n = 3 replicates) (100 to 150 cells counted per well). The data shown are representative of three independent experiments. (c) Purified rabbit osteoclasts were treated for 48 hours with 100 μM ALN ± 100 ng/mL RANKL or with RANKL alone. Cell lysates were then analysed by Western blotting for the unprenylated form of Rap1A and for β-actin. (d) Purified rabbit osteoclasts were treated for 48 hours with 100 μM ALN ± 100 ng/mL RANKL or with 100 ng/mL RANKL alone. Cell lysates were then analysed by Western blotting for Mcl-1 and Bcl-2. The level of Mcl-2 or Bcl-2 was quantified by densitometric analysis and expressed as a ratio of the level in control cells. Data shown are representative of three independent experiments. ALN, 4-amino-1-hydroxy-butylidene-1,1-bisphosphonate (alendronate); RANKL, receptor activator of nuclear factor-kappa-B ligand.
Figure Legend Snippet: RANKL prevents activation of caspase-9 and increases Mcl-1 in osteoclasts but does not prevent inhibition of protein prenylation. Cultures of mature osteoclasts from rabbit bones were treated with 100 μM ALN ± 100 ng/mL RANKL for 48 hours and stained using an Apofluor Green Caspase-9 Activity Assay kit and Hoechst 33342. (a) A representative non-apoptotic and apoptotic osteoclast. (b) Quantification of caspase-9-positive osteoclasts after treatment with alendronate ± RANKL for 48 hours. * P ≤ 0.05 compared with ALN alone or # P ≤ 0.05 compared with control (CTL) (analysis of variance). Values are the mean ± standard error of the mean (n = 3 replicates) (100 to 150 cells counted per well). The data shown are representative of three independent experiments. (c) Purified rabbit osteoclasts were treated for 48 hours with 100 μM ALN ± 100 ng/mL RANKL or with RANKL alone. Cell lysates were then analysed by Western blotting for the unprenylated form of Rap1A and for β-actin. (d) Purified rabbit osteoclasts were treated for 48 hours with 100 μM ALN ± 100 ng/mL RANKL or with 100 ng/mL RANKL alone. Cell lysates were then analysed by Western blotting for Mcl-1 and Bcl-2. The level of Mcl-2 or Bcl-2 was quantified by densitometric analysis and expressed as a ratio of the level in control cells. Data shown are representative of three independent experiments. ALN, 4-amino-1-hydroxy-butylidene-1,1-bisphosphonate (alendronate); RANKL, receptor activator of nuclear factor-kappa-B ligand.

Techniques Used: Activation Assay, Inhibition, Staining, Activity Assay, CTL Assay, Purification, Western Blot

Mcl-1 levels decrease rapidly in mouse osteoclasts following cytokine starvation but are restored by pro-survival factors. Mouse osteoclasts were generated by culturing bone marrow macrophages for 5 days with macrophage colony-stimulating factor (M-CSF) + receptor activator of nuclear factor-kappa-B ligand (RANKL). (a) Osteoclasts were starved of M-CSF and RANKL for 8 hours and then fixed and processed for scanning EM analysis. Representative osteoclasts from non-starved (control) or starved cultures are shown. Bars = 10 μm. (b) Mouse osteoclasts were starved of M-CSF and RANKL for 2 to 12 hours. Western blot analysis was then used to determine the level of Mcl-1, cleaved caspase-3, Bcl-2, and Bcl-x L at each time point. (c) After osteoclasts were generated, the medium was replaced with normal medium (control [Ctrl]: M-CSF + RANKL), with medium lacking cytokines (starved), or with medium containing recombinant M-CSF, RANKL, tumour necrosis factor-alpha (TNF-α), or lipopolysaccharide (LPS). After 12 hours, Western blotting was used to determine the level of Mcl-1 in 40 μg of cell lysate. Data shown are representative of three independent experiments.
Figure Legend Snippet: Mcl-1 levels decrease rapidly in mouse osteoclasts following cytokine starvation but are restored by pro-survival factors. Mouse osteoclasts were generated by culturing bone marrow macrophages for 5 days with macrophage colony-stimulating factor (M-CSF) + receptor activator of nuclear factor-kappa-B ligand (RANKL). (a) Osteoclasts were starved of M-CSF and RANKL for 8 hours and then fixed and processed for scanning EM analysis. Representative osteoclasts from non-starved (control) or starved cultures are shown. Bars = 10 μm. (b) Mouse osteoclasts were starved of M-CSF and RANKL for 2 to 12 hours. Western blot analysis was then used to determine the level of Mcl-1, cleaved caspase-3, Bcl-2, and Bcl-x L at each time point. (c) After osteoclasts were generated, the medium was replaced with normal medium (control [Ctrl]: M-CSF + RANKL), with medium lacking cytokines (starved), or with medium containing recombinant M-CSF, RANKL, tumour necrosis factor-alpha (TNF-α), or lipopolysaccharide (LPS). After 12 hours, Western blotting was used to determine the level of Mcl-1 in 40 μg of cell lysate. Data shown are representative of three independent experiments.

Techniques Used: Generated, Western Blot, Recombinant

20) Product Images from "Buthionine sulfoximine sensitizes antihormone-resistant human breast cancer cells to estrogen-induced apoptosis"

Article Title: Buthionine sulfoximine sensitizes antihormone-resistant human breast cancer cells to estrogen-induced apoptosis

Journal: Breast Cancer Research : BCR

doi: 10.1186/bcr2208

Effect of buthionine sulfoximine (BSO) and 17β-estradiol (E 2 ) on Bcl-2 family protein expression and mitochondrial function in MCF-7 and MCF-7:2A cells. (a) Western blot analysis for pBcl-2, Bcl-2, Bcl-x L , and Bax protein expression in parental MCF-7 cells and MCF-7:2A cells following 48 h of treatment with ethanol vehicle (Control), 1 nM E 2 , 100 μM BSO, or E 2 + BSO. Equal loading was confirmed by reprobing with an antibody against β-actin. (b) Small interfering RNA (siRNA) knockdown of Bcl-2 partially sensitizes MCF-7:2A cells to E 2 -induced apoptosis. Cells were transfected with 100 nM siRNA-Bcl-2 or siRNA-Con (control) and expression levels of Bcl-2 was determined by immunoblot analysis (top). Annexin V staining (bottom) showing the effects of siRNA-con and siRNA-Bcl-2 on apoptosis induced by estradiol treatment in MCF-7:2A cells. *, p
Figure Legend Snippet: Effect of buthionine sulfoximine (BSO) and 17β-estradiol (E 2 ) on Bcl-2 family protein expression and mitochondrial function in MCF-7 and MCF-7:2A cells. (a) Western blot analysis for pBcl-2, Bcl-2, Bcl-x L , and Bax protein expression in parental MCF-7 cells and MCF-7:2A cells following 48 h of treatment with ethanol vehicle (Control), 1 nM E 2 , 100 μM BSO, or E 2 + BSO. Equal loading was confirmed by reprobing with an antibody against β-actin. (b) Small interfering RNA (siRNA) knockdown of Bcl-2 partially sensitizes MCF-7:2A cells to E 2 -induced apoptosis. Cells were transfected with 100 nM siRNA-Bcl-2 or siRNA-Con (control) and expression levels of Bcl-2 was determined by immunoblot analysis (top). Annexin V staining (bottom) showing the effects of siRNA-con and siRNA-Bcl-2 on apoptosis induced by estradiol treatment in MCF-7:2A cells. *, p

Techniques Used: Expressing, Western Blot, Small Interfering RNA, Transfection, Staining

21) Product Images from "Buthionine sulfoximine sensitizes antihormone-resistant human breast cancer cells to estrogen-induced apoptosis"

Article Title: Buthionine sulfoximine sensitizes antihormone-resistant human breast cancer cells to estrogen-induced apoptosis

Journal: Breast Cancer Research : BCR

doi: 10.1186/bcr2208

Effect of buthionine sulfoximine (BSO) and 17β-estradiol (E 2 ) on Bcl-2 family protein expression and mitochondrial function in MCF-7 and MCF-7:2A cells. (a) Western blot analysis for pBcl-2, Bcl-2, Bcl-x L , and Bax protein expression in parental MCF-7 cells and MCF-7:2A cells following 48 h of treatment with ethanol vehicle (Control), 1 nM E 2 , 100 μM BSO, or E 2 + BSO. Equal loading was confirmed by reprobing with an antibody against β-actin. (b) Small interfering RNA (siRNA) knockdown of Bcl-2 partially sensitizes MCF-7:2A cells to E 2 -induced apoptosis. Cells were transfected with 100 nM siRNA-Bcl-2 or siRNA-Con (control) and expression levels of Bcl-2 was determined by immunoblot analysis (top). Annexin V staining (bottom) showing the effects of siRNA-con and siRNA-Bcl-2 on apoptosis induced by estradiol treatment in MCF-7:2A cells. *, p
Figure Legend Snippet: Effect of buthionine sulfoximine (BSO) and 17β-estradiol (E 2 ) on Bcl-2 family protein expression and mitochondrial function in MCF-7 and MCF-7:2A cells. (a) Western blot analysis for pBcl-2, Bcl-2, Bcl-x L , and Bax protein expression in parental MCF-7 cells and MCF-7:2A cells following 48 h of treatment with ethanol vehicle (Control), 1 nM E 2 , 100 μM BSO, or E 2 + BSO. Equal loading was confirmed by reprobing with an antibody against β-actin. (b) Small interfering RNA (siRNA) knockdown of Bcl-2 partially sensitizes MCF-7:2A cells to E 2 -induced apoptosis. Cells were transfected with 100 nM siRNA-Bcl-2 or siRNA-Con (control) and expression levels of Bcl-2 was determined by immunoblot analysis (top). Annexin V staining (bottom) showing the effects of siRNA-con and siRNA-Bcl-2 on apoptosis induced by estradiol treatment in MCF-7:2A cells. *, p

Techniques Used: Expressing, Western Blot, Small Interfering RNA, Transfection, Staining

22) Product Images from "The neuroprotective effect of recombinant human erythropoietin via an antiapoptotic mechanism on hypoxic-ischemic brain injury in neonatal rats"

Article Title: The neuroprotective effect of recombinant human erythropoietin via an antiapoptotic mechanism on hypoxic-ischemic brain injury in neonatal rats

Journal: Korean Journal of Pediatrics

doi: 10.3345/kjp.2010.53.10.898

Western blots of Bcl-2 (A; N, 100±0; H, 97.6±0.96; H+E1, 95.2±0.45; H+E10, 102.9±0.75; H+E100, 98.7±0.85), Bax (B; N, 100±0; H, 104.3±0.57; H+E1, 97.7±0.7; H+E10, 91±0.87; H+E100, 84.3±0.54), and caspase-3 (C, N, 100±0; H, 107.8±0.71; H+E1, 99.2±0.63; H+E10, 104.6±0.89; H+E100, 126.9±0.61) in cultured cortical neuronal cells from 19-day-old rat embryos, and the ratio of Bax/Bcl-2 expression (D). Recombinant human erythropoietin (rHuEPO) was administered at 1, 10, and 100 IU/mL. A, Normoxia group (N, n=4); B, Hypoxia group (H, n=4); C, Hhypoxia+1 IU/mL rHuEPO-treated group (H+E1, n=4); D, Hypoxia+10 IU/mL rHuEPO-treated group (H+E10, n=4); E, Hypoxia+100 IU/mL rHuEPO-treated group (H+E100, n=4). * P
Figure Legend Snippet: Western blots of Bcl-2 (A; N, 100±0; H, 97.6±0.96; H+E1, 95.2±0.45; H+E10, 102.9±0.75; H+E100, 98.7±0.85), Bax (B; N, 100±0; H, 104.3±0.57; H+E1, 97.7±0.7; H+E10, 91±0.87; H+E100, 84.3±0.54), and caspase-3 (C, N, 100±0; H, 107.8±0.71; H+E1, 99.2±0.63; H+E10, 104.6±0.89; H+E100, 126.9±0.61) in cultured cortical neuronal cells from 19-day-old rat embryos, and the ratio of Bax/Bcl-2 expression (D). Recombinant human erythropoietin (rHuEPO) was administered at 1, 10, and 100 IU/mL. A, Normoxia group (N, n=4); B, Hypoxia group (H, n=4); C, Hhypoxia+1 IU/mL rHuEPO-treated group (H+E1, n=4); D, Hypoxia+10 IU/mL rHuEPO-treated group (H+E10, n=4); E, Hypoxia+100 IU/mL rHuEPO-treated group (H+E100, n=4). * P

Techniques Used: Western Blot, Cell Culture, Expressing, Recombinant

Western blots of Bcl-2 (A, NC, 100±0; NS, 104.8±1.0; H, 90.4±1.14; HV, 87.9±0.56; HE-B, 112±1.12; HE-A, 102.8±0.37), Bax (B, NC, 100±0; NS, 100.3±0.73; H, 113.7±1.23; HV, 115.9±1.08; HE-B, 105.7±1.48; HE-A, 104.9±1.07), and caspase-3 (C, NC, 100±0; NS, 100.9±0.41; H, 116.9±1.57; HV, 118.5±1.76; HE-B, 107.2±1.63; HE-A (105.9±2.51) antibodies 7 days after hypoxic insult, and the ratio of Bax/Bcl-2 expression (D). Recombinant human erythropoietin (rHuEPO) was administered intraperitoneally at 1,000 IU/kg. NC, Normoxia control group (n=7); NS, Normoxia sham-operated group (n=8); H, Hypoxia group (n=8); HV, Hypoxia+Vehicle group (n=7); HE-B, Hypoxia+rHuEPO-treated group before hypoxic insult (n=8); HE-A, Hypoxia+rHuEPO-treated group after hypoxic insult (n=8). * P
Figure Legend Snippet: Western blots of Bcl-2 (A, NC, 100±0; NS, 104.8±1.0; H, 90.4±1.14; HV, 87.9±0.56; HE-B, 112±1.12; HE-A, 102.8±0.37), Bax (B, NC, 100±0; NS, 100.3±0.73; H, 113.7±1.23; HV, 115.9±1.08; HE-B, 105.7±1.48; HE-A, 104.9±1.07), and caspase-3 (C, NC, 100±0; NS, 100.9±0.41; H, 116.9±1.57; HV, 118.5±1.76; HE-B, 107.2±1.63; HE-A (105.9±2.51) antibodies 7 days after hypoxic insult, and the ratio of Bax/Bcl-2 expression (D). Recombinant human erythropoietin (rHuEPO) was administered intraperitoneally at 1,000 IU/kg. NC, Normoxia control group (n=7); NS, Normoxia sham-operated group (n=8); H, Hypoxia group (n=8); HV, Hypoxia+Vehicle group (n=7); HE-B, Hypoxia+rHuEPO-treated group before hypoxic insult (n=8); HE-A, Hypoxia+rHuEPO-treated group after hypoxic insult (n=8). * P

Techniques Used: Western Blot, Expressing, Recombinant

Real-time PCR of Bcl-2 (A; NC, 100±0; NS, 91.4±2.63; H, 80.7±1.1; HV, 77.4±1.39; HE-B, 118.1±1.63; HE-A, 115.7±2.32), Bax (B; NC, 100±0; NS, 100.7±0.51; H, 111.7±0.6; HV, 110.9±1.24; HE-B, 104.2±0.97; HE-A, 98.6±1.35), and caspase-3 (C; NC, 100±0; NS, 116.5±1.23; H, 135.7±2.8; HV, 139.5±1.11; HE-B, 97.3±0.68; HE-A, 102.1±0.74) primers 7 days after hypoxic insult, and the ratio of Bax/Bcl-2 expression (D). Recombinant human erythropoietin (rHuEPO) was administered intraperitoneally at 1,000 IU/kg. NC, Normoxia control group (n=7); NS, Normoxia sham-operated group (n=8); H, Hypoxia group (n=8); HV, Hypoxia+Vehicle group (n=7); HE-B, Hypoxia+rHuEPO-treated group before hypoxic insult (n=8); HE-A, Hypoxia+rHuEPO-treated group after hypoxic insult (n=8). * P
Figure Legend Snippet: Real-time PCR of Bcl-2 (A; NC, 100±0; NS, 91.4±2.63; H, 80.7±1.1; HV, 77.4±1.39; HE-B, 118.1±1.63; HE-A, 115.7±2.32), Bax (B; NC, 100±0; NS, 100.7±0.51; H, 111.7±0.6; HV, 110.9±1.24; HE-B, 104.2±0.97; HE-A, 98.6±1.35), and caspase-3 (C; NC, 100±0; NS, 116.5±1.23; H, 135.7±2.8; HV, 139.5±1.11; HE-B, 97.3±0.68; HE-A, 102.1±0.74) primers 7 days after hypoxic insult, and the ratio of Bax/Bcl-2 expression (D). Recombinant human erythropoietin (rHuEPO) was administered intraperitoneally at 1,000 IU/kg. NC, Normoxia control group (n=7); NS, Normoxia sham-operated group (n=8); H, Hypoxia group (n=8); HV, Hypoxia+Vehicle group (n=7); HE-B, Hypoxia+rHuEPO-treated group before hypoxic insult (n=8); HE-A, Hypoxia+rHuEPO-treated group after hypoxic insult (n=8). * P

Techniques Used: Real-time Polymerase Chain Reaction, Expressing, Recombinant

Real-time PCR of Bcl-2 (A; N, 100±0; H, 86.5±0.84; H+E1, 110.2±2.1; H+E10, 76.8±1.38; H+E100, 91.4±0.98), Bax (B; N, 100±0; H, 123.9±1.31; H+E, 1,115.7±1.6; H+E10, 102.1±1.89; H+E100, 116.5±0.82), and caspase-3 (C; N, 100±0; H, 135.7±0.79; H+E1, 126.6±1.16; H+E10, 88.9±0.69; H+E100, 134.7±0.74) mRNAs in cultured cortical neuronal cells from 19-day-old rat embryos, and the ratio of Bax/Bcl-2 expression (D). Recombinant human erythropoietin (rHuEPO) was administered at 1, 10, and 100 IU/mL. A, Normoxia group (N, n=4); B, Hypoxia group (H, n=4); C, Hypoxia +1 IU/mL rHuEPO-treated group (H+E1, n=4); D, Hypoxia+10 IU/mL rHuEPO-treated group (H+E10, n=4); E, Hypoxia+100 IU/mL rHuEPO-treated group (H+E100, n=4). * P
Figure Legend Snippet: Real-time PCR of Bcl-2 (A; N, 100±0; H, 86.5±0.84; H+E1, 110.2±2.1; H+E10, 76.8±1.38; H+E100, 91.4±0.98), Bax (B; N, 100±0; H, 123.9±1.31; H+E, 1,115.7±1.6; H+E10, 102.1±1.89; H+E100, 116.5±0.82), and caspase-3 (C; N, 100±0; H, 135.7±0.79; H+E1, 126.6±1.16; H+E10, 88.9±0.69; H+E100, 134.7±0.74) mRNAs in cultured cortical neuronal cells from 19-day-old rat embryos, and the ratio of Bax/Bcl-2 expression (D). Recombinant human erythropoietin (rHuEPO) was administered at 1, 10, and 100 IU/mL. A, Normoxia group (N, n=4); B, Hypoxia group (H, n=4); C, Hypoxia +1 IU/mL rHuEPO-treated group (H+E1, n=4); D, Hypoxia+10 IU/mL rHuEPO-treated group (H+E10, n=4); E, Hypoxia+100 IU/mL rHuEPO-treated group (H+E100, n=4). * P

Techniques Used: Real-time Polymerase Chain Reaction, Cell Culture, Expressing, Recombinant

23) Product Images from "An in vitro endothelial cell protective effect of secretory leukocyte protease inhibitor against simulated ischaemia/reperfusion injury"

Article Title: An in vitro endothelial cell protective effect of secretory leukocyte protease inhibitor against simulated ischaemia/reperfusion injury

Journal: Experimental and Therapeutic Medicine

doi: 10.3892/etm.2017.5272

(A) Effects of rhSLPI on the activation of apoptotic regulatory proteins. HUVECs were subjected to control medium incubation, 20-min sI, or 1,000 ng/ml rhSLPI prior to ischaemia. Endothelial cell proteins were prepared for western blot analysis to detect the expression levels of Bax, Bcl-2 and cleaved caspase 3. (B) Quantified levels of Bax, Bcl-2, Bax: Bcl-2 ratio and cleaved caspase 3 were detected in 3–6 experiments with independent cell preparations. *P
Figure Legend Snippet: (A) Effects of rhSLPI on the activation of apoptotic regulatory proteins. HUVECs were subjected to control medium incubation, 20-min sI, or 1,000 ng/ml rhSLPI prior to ischaemia. Endothelial cell proteins were prepared for western blot analysis to detect the expression levels of Bax, Bcl-2 and cleaved caspase 3. (B) Quantified levels of Bax, Bcl-2, Bax: Bcl-2 ratio and cleaved caspase 3 were detected in 3–6 experiments with independent cell preparations. *P

Techniques Used: Activation Assay, Incubation, Western Blot, Expressing

24) Product Images from "Potential Role of Thymosin-α1 Adjuvant Therapy for Glioblastoma"

Article Title: Potential Role of Thymosin-α1 Adjuvant Therapy for Glioblastoma

Journal: Journal of Oncology

doi: 10.1155/2009/302084

Increased proapoptosis gene products in Talpha1-treated 9L glioblastoma cells. 9L cells seeded in 96-well plates were treated with 10 mM Talpha1 for 24 hours. After fixation and permeabilization, immunoreactivity was measured directly in the cells using the microtiter immunocytochemical ELISA (MICE) assay. Levels of immunoreactivity were normalized to cell density and the corresponding ratio represents the MICE index. The graph depicts the mean ± S.D. of the levels of proliferating cell nuclear antigen (PCNA), Bcl-2, p21, p53, Fas L, Fas R, tumor necrosis factor receptor, type 1 (TNF R1), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) measured in 8 replicate vehicle-treated or Talpha1-treated cultures. Asterisks denote significant differences from control ( P
Figure Legend Snippet: Increased proapoptosis gene products in Talpha1-treated 9L glioblastoma cells. 9L cells seeded in 96-well plates were treated with 10 mM Talpha1 for 24 hours. After fixation and permeabilization, immunoreactivity was measured directly in the cells using the microtiter immunocytochemical ELISA (MICE) assay. Levels of immunoreactivity were normalized to cell density and the corresponding ratio represents the MICE index. The graph depicts the mean ± S.D. of the levels of proliferating cell nuclear antigen (PCNA), Bcl-2, p21, p53, Fas L, Fas R, tumor necrosis factor receptor, type 1 (TNF R1), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) measured in 8 replicate vehicle-treated or Talpha1-treated cultures. Asterisks denote significant differences from control ( P

Techniques Used: Enzyme-linked Immunosorbent Assay, Mouse Assay

25) Product Images from "Protective Effects of Hesperidin (Citrus Flavonone) on High Glucose Induced Oxidative Stress and Apoptosis in a Cellular Model for Diabetic Retinopathy"

Article Title: Protective Effects of Hesperidin (Citrus Flavonone) on High Glucose Induced Oxidative Stress and Apoptosis in a Cellular Model for Diabetic Retinopathy

Journal: Nutrients

doi: 10.3390/nu9121312

Effects of hesperidin on protein expression related to apoptosis in RGC-5 cells under high glucose conditions. The RGCs were cultured with normal (NG) or high glucose (HG) plus hesperidin at concentrations of 12.5 (Hesp 12.5), 25 (Hesp 25), or 50 μmol/L (Hesp 50) for 48 h. ( A ) Protein bands of cleaved caspase-9 and cleaved caspase-3 in RGC-5 cells detected by Western blotting; ( B ) Quantitative densitometric analysis of caspase-9 and cleaved caspase-3; ( C ) Protein bands of Bax and Bcl-2 in RGC-5 cells detected by Western blotting; ( D ) Changes of the ratios of Bax/Bcl-2 are displayed in the bottom panel. The results are presented as the mean ± SD of five independent experiments ( n = 5), each of which was performed in triplicate. a p
Figure Legend Snippet: Effects of hesperidin on protein expression related to apoptosis in RGC-5 cells under high glucose conditions. The RGCs were cultured with normal (NG) or high glucose (HG) plus hesperidin at concentrations of 12.5 (Hesp 12.5), 25 (Hesp 25), or 50 μmol/L (Hesp 50) for 48 h. ( A ) Protein bands of cleaved caspase-9 and cleaved caspase-3 in RGC-5 cells detected by Western blotting; ( B ) Quantitative densitometric analysis of caspase-9 and cleaved caspase-3; ( C ) Protein bands of Bax and Bcl-2 in RGC-5 cells detected by Western blotting; ( D ) Changes of the ratios of Bax/Bcl-2 are displayed in the bottom panel. The results are presented as the mean ± SD of five independent experiments ( n = 5), each of which was performed in triplicate. a p

Techniques Used: Expressing, Cell Culture, Western Blot

26) Product Images from "Herpesvirus Saimiri Transforms Human T-Cell Clones to Stable Growth without Inducing Resistance to Apoptosis"

Article Title: Herpesvirus Saimiri Transforms Human T-Cell Clones to Stable Growth without Inducing Resistance to Apoptosis

Journal: Journal of Virology

doi:

Differential expression of HVS- bcl-2 and HVS- flip . (A) Total RNA of the indicated cell lines was loaded. OMK cells were infected with HVS C488 or left uninfected. The transformed T-cell line 93C488 from Saguinus fuscicollis had stopped releasing infectious virus and remained a nonproducer of infectious virus even after stimulation with PMA, while the HVS-transformed T-cell line P1081 from Callithrix jacchus produced infectious virus. Like all studied human T-cell lines, the CB-15 cell line did not produce infectious virus, either before or after activation with PMA. The top panel shows the transcripts of HVS- bcl-2 , the middle panel shows the transcripts of HVS- flip , and the bottom panel shows the corresponding rRNA as detected by ethidium bromide staining. Three pieces of the same Northern blot are shown. (B) Poly(A) + RNA of the two human transformed T-cell lines CB-15 and ES-BP8T and RNA of lytically infected OMK cells were analyzed. The bottom panel shows the hybridization with a gapdh probe. In the top panel of both A and B, the bands at 1.1, 1.8, and ca. 5 kb are specifically detected by the HVS- bcl-2 probe. In the middle panel of A and B, the bands at 5 and 7.5 kb are specific for HVS- flip.
Figure Legend Snippet: Differential expression of HVS- bcl-2 and HVS- flip . (A) Total RNA of the indicated cell lines was loaded. OMK cells were infected with HVS C488 or left uninfected. The transformed T-cell line 93C488 from Saguinus fuscicollis had stopped releasing infectious virus and remained a nonproducer of infectious virus even after stimulation with PMA, while the HVS-transformed T-cell line P1081 from Callithrix jacchus produced infectious virus. Like all studied human T-cell lines, the CB-15 cell line did not produce infectious virus, either before or after activation with PMA. The top panel shows the transcripts of HVS- bcl-2 , the middle panel shows the transcripts of HVS- flip , and the bottom panel shows the corresponding rRNA as detected by ethidium bromide staining. Three pieces of the same Northern blot are shown. (B) Poly(A) + RNA of the two human transformed T-cell lines CB-15 and ES-BP8T and RNA of lytically infected OMK cells were analyzed. The bottom panel shows the hybridization with a gapdh probe. In the top panel of both A and B, the bands at 1.1, 1.8, and ca. 5 kb are specifically detected by the HVS- bcl-2 probe. In the middle panel of A and B, the bands at 5 and 7.5 kb are specific for HVS- flip.

Techniques Used: Expressing, Infection, Transformation Assay, Produced, Activation Assay, Staining, Northern Blot, Hybridization

Expression of Bcl-2, Bcl-X, and Bax. The uninfected parental T-cell clone ES-BP8 (lanes 1) and its HVS-transformed derivative ES-BP8T (lanes 2) were analysed by Western blotting (A) and flow cytometry (B). (A) Aliquots containing 20 μg of total protein were used to detect Bcl-2 or Bcl-X, and 5 μg of total protein was loaded to detect Bax. The positions of prestained molecular mass markers are indicated in kilodaltons. (B) Staining of the native clone ES-BP8 is labeled 1, and staining of the transformed clone is labeled with 2. The open graph represents the negative control, and the solid graph represents the specific staining.
Figure Legend Snippet: Expression of Bcl-2, Bcl-X, and Bax. The uninfected parental T-cell clone ES-BP8 (lanes 1) and its HVS-transformed derivative ES-BP8T (lanes 2) were analysed by Western blotting (A) and flow cytometry (B). (A) Aliquots containing 20 μg of total protein were used to detect Bcl-2 or Bcl-X, and 5 μg of total protein was loaded to detect Bax. The positions of prestained molecular mass markers are indicated in kilodaltons. (B) Staining of the native clone ES-BP8 is labeled 1, and staining of the transformed clone is labeled with 2. The open graph represents the negative control, and the solid graph represents the specific staining.

Techniques Used: Expressing, Transformation Assay, Western Blot, Flow Cytometry, Cytometry, Staining, Labeling, Negative Control

27) Product Images from "Human Parvovirus B19 Nonstructural (NS1) Protein Induces Apoptosis in Erythroid Lineage Cells"

Article Title: Human Parvovirus B19 Nonstructural (NS1) Protein Induces Apoptosis in Erythroid Lineage Cells

Journal: Journal of Virology

doi:

Stable expression of human Bcl-2 significantly reduces NS1-induced cell death. (A) Representative Bcl-2-stable transfectants of both KLNS and ULNS cells were detected with a Bcl-2 MAb, Bcl-2 100, by immunoblotting with 5 × 10 6 cells in the presence or absence of IPTG. The position of the Bcl-2 protein corresponding to approximately 26 kDa is indicated. (B and C) The kinetics of Bcl-2 inhibition of NS1-induced cell death was measured by trypan blue exclusion for both KLNS (B) and ULNS (C) cells with 5 × 10 5 cells for each cell line. The experiments were performed twice, with no significant difference between results.
Figure Legend Snippet: Stable expression of human Bcl-2 significantly reduces NS1-induced cell death. (A) Representative Bcl-2-stable transfectants of both KLNS and ULNS cells were detected with a Bcl-2 MAb, Bcl-2 100, by immunoblotting with 5 × 10 6 cells in the presence or absence of IPTG. The position of the Bcl-2 protein corresponding to approximately 26 kDa is indicated. (B and C) The kinetics of Bcl-2 inhibition of NS1-induced cell death was measured by trypan blue exclusion for both KLNS (B) and ULNS (C) cells with 5 × 10 5 cells for each cell line. The experiments were performed twice, with no significant difference between results.

Techniques Used: Expressing, Inhibition

28) Product Images from "Human Parvovirus B19 Nonstructural (NS1) Protein Induces Apoptosis in Erythroid Lineage Cells"

Article Title: Human Parvovirus B19 Nonstructural (NS1) Protein Induces Apoptosis in Erythroid Lineage Cells

Journal: Journal of Virology

doi:

Stable expression of human Bcl-2 significantly reduces NS1-induced cell death. (A) Representative Bcl-2-stable transfectants of both KLNS and ULNS cells were detected with a Bcl-2 MAb, Bcl-2 100, by immunoblotting with 5 × 10 6 cells in the presence or absence of IPTG. The position of the Bcl-2 protein corresponding to approximately 26 kDa is indicated. (B and C) The kinetics of Bcl-2 inhibition of NS1-induced cell death was measured by trypan blue exclusion for both KLNS (B) and ULNS (C) cells with 5 × 10 5 cells for each cell line. The experiments were performed twice, with no significant difference between results.
Figure Legend Snippet: Stable expression of human Bcl-2 significantly reduces NS1-induced cell death. (A) Representative Bcl-2-stable transfectants of both KLNS and ULNS cells were detected with a Bcl-2 MAb, Bcl-2 100, by immunoblotting with 5 × 10 6 cells in the presence or absence of IPTG. The position of the Bcl-2 protein corresponding to approximately 26 kDa is indicated. (B and C) The kinetics of Bcl-2 inhibition of NS1-induced cell death was measured by trypan blue exclusion for both KLNS (B) and ULNS (C) cells with 5 × 10 5 cells for each cell line. The experiments were performed twice, with no significant difference between results.

Techniques Used: Expressing, Inhibition

29) Product Images from "Suppression of pancreatic beta cell apoptosis by Danzhi Jiangtang capsule contributes to the attenuation of type 1 diabetes in rats"

Article Title: Suppression of pancreatic beta cell apoptosis by Danzhi Jiangtang capsule contributes to the attenuation of type 1 diabetes in rats

Journal: BMC Complementary and Alternative Medicine

doi: 10.1186/s12906-016-0993-4

Effect of DJC on Bcl-2 protein level in rat pancreas. Six randomly selected islets of each section were analyzed for mean optical density and averaged to serve as the expression level of each animal. Data were presented as mean ± SD ( n = 9 in Model group, n = 10 in the other groups). a - d : Representative microphotographs of immunohistochemical examination of Bcl-2 protein (×400). a : Control group; b : Model group; c : DJCH group; d : DJCL group. e : Quantitative analysis of Bcl-2 protein level. ** P
Figure Legend Snippet: Effect of DJC on Bcl-2 protein level in rat pancreas. Six randomly selected islets of each section were analyzed for mean optical density and averaged to serve as the expression level of each animal. Data were presented as mean ± SD ( n = 9 in Model group, n = 10 in the other groups). a - d : Representative microphotographs of immunohistochemical examination of Bcl-2 protein (×400). a : Control group; b : Model group; c : DJCH group; d : DJCL group. e : Quantitative analysis of Bcl-2 protein level. ** P

Techniques Used: Expressing, Immunohistochemistry

Western blot analysis of pancreatic levels of Bax and Bcl-2. Total protein were extracted from pancreas and subjected to western blot analysis. Levels of Bax and Bcl-2 protein were normalized to that of β-actin. Data were presented as percentage of that in Control group (Mean ± SD, n = 5). ** P
Figure Legend Snippet: Western blot analysis of pancreatic levels of Bax and Bcl-2. Total protein were extracted from pancreas and subjected to western blot analysis. Levels of Bax and Bcl-2 protein were normalized to that of β-actin. Data were presented as percentage of that in Control group (Mean ± SD, n = 5). ** P

Techniques Used: Western Blot

30) Product Images from "Reactivation of Smac-mediated apoptosis in chronic lymphocytic leukemia cells: mechanistic studies of Smac mimetic"

Article Title: Reactivation of Smac-mediated apoptosis in chronic lymphocytic leukemia cells: mechanistic studies of Smac mimetic

Journal: Oncotarget

doi: 10.18632/oncotarget.8462

Degradation of IAPs and activation of caspases (8, 9, and 3) following smac066 treatment A.-B. Primary CLL cells were untreated or treated with smac066 (S) (5 μM). A. IAPs (XIAP, cIAP1 and anti-apoptotic Mcl-1) B. cIAP1 and anti-apoptotic family Bcl-2, and Bcl-xL were evaluated by immunoblotting analysis. Pt = patient; C = untreated CLL; S = smac066. C. Additional samples were evaluated in a similar fashion ( n = 8). The specific bands for XIAP and cIAP2 are indicated by arrows. Prognosis and percent viable cells determined by annexin V/PI binding assay for each sample is provided. The blots originated from the same gel (the membrane is either cut into different pieces according to kD of the protein or probed with two antibodies (XIAP and cIAP2) of different species (rabbit/mouse) at the same time; this is technically feasible with LI-COR Odyssey infrared imager. D. - F. Quantitation of immunoblots (3C) for XIAP, cIAP2, and Mcl-1, normalized to GAPDH levels. G. - I. Correlation between percent viable cells and protein levels of XIAP, cIAP2, and Mcl-1 following 24-hr treatment with smac066 (5 μM; n = 8). The r 2 on the correlation is obtained through linear regression analysis. J. Primary CLL cells were untreated or treated with smac066 (S) (5 μM) for 24 hr and caspase cleavages were measured by immunoblotting analysis. GAPDH was used as a loading control. Prognosis and percent viable cells determined by annexin V/PI binding assay for each sample is provided. The ratio between the protein of interest and its respective GAPDH is set as 100%. C = untreated CLL. K. - M. Correlation between percent apoptosis and caspase cleavage (caspases 8, 9 and 3) following smac066 treatment (5 μM; 24 hr). The r 2 on the correlation is obtained through linear regression analysis.
Figure Legend Snippet: Degradation of IAPs and activation of caspases (8, 9, and 3) following smac066 treatment A.-B. Primary CLL cells were untreated or treated with smac066 (S) (5 μM). A. IAPs (XIAP, cIAP1 and anti-apoptotic Mcl-1) B. cIAP1 and anti-apoptotic family Bcl-2, and Bcl-xL were evaluated by immunoblotting analysis. Pt = patient; C = untreated CLL; S = smac066. C. Additional samples were evaluated in a similar fashion ( n = 8). The specific bands for XIAP and cIAP2 are indicated by arrows. Prognosis and percent viable cells determined by annexin V/PI binding assay for each sample is provided. The blots originated from the same gel (the membrane is either cut into different pieces according to kD of the protein or probed with two antibodies (XIAP and cIAP2) of different species (rabbit/mouse) at the same time; this is technically feasible with LI-COR Odyssey infrared imager. D. - F. Quantitation of immunoblots (3C) for XIAP, cIAP2, and Mcl-1, normalized to GAPDH levels. G. - I. Correlation between percent viable cells and protein levels of XIAP, cIAP2, and Mcl-1 following 24-hr treatment with smac066 (5 μM; n = 8). The r 2 on the correlation is obtained through linear regression analysis. J. Primary CLL cells were untreated or treated with smac066 (S) (5 μM) for 24 hr and caspase cleavages were measured by immunoblotting analysis. GAPDH was used as a loading control. Prognosis and percent viable cells determined by annexin V/PI binding assay for each sample is provided. The ratio between the protein of interest and its respective GAPDH is set as 100%. C = untreated CLL. K. - M. Correlation between percent apoptosis and caspase cleavage (caspases 8, 9 and 3) following smac066 treatment (5 μM; 24 hr). The r 2 on the correlation is obtained through linear regression analysis.

Techniques Used: Activation Assay, Binding Assay, Quantitation Assay, Western Blot

Effect of pan-caspase inhibitor Z-VAD-fmk on smac066-induced apoptosis A. CLL primary cells were incubated with smac066 (S) in the presence or absence of Z-VAD-fmk (Z), and percent viable cells was determined by annexin/PI binding assay ( n = 12). The given p values are derived from paired t -test analyzed using Graph Pad Prizm. The horizontal lines denote median values. C = untreated CLL. B. - C. Protein levels of IAPs (XIAP, cIAP1, and cIAP2) and Bcl-2 family anti-apoptotic proteins (Bcl-2, Mcl-1, and Bcl-xL) were determined by immunoblotting. Pt 67a-d denotes that this patient arrived twice to the clinic and the immunoblot analyses were done twice. GAPDH was used as a loading control. D. Mouse embryo fibroblasts for wild-type (WT) or double-knockout (DKO) Bax/Bak were incubated without or with various concentrations of smac066 for 24 hr ( n = 3). Percent viable cells were determined by annexin/PI binding assay ( n = 3; error bars denote mean ± SEM), and percent growth inhibition was determined by the cell counting method ( n = 3; one representative data is produced). The data are expressed as percent relative to control (untreated cells). DMSO = dimethyl sulfoxide.
Figure Legend Snippet: Effect of pan-caspase inhibitor Z-VAD-fmk on smac066-induced apoptosis A. CLL primary cells were incubated with smac066 (S) in the presence or absence of Z-VAD-fmk (Z), and percent viable cells was determined by annexin/PI binding assay ( n = 12). The given p values are derived from paired t -test analyzed using Graph Pad Prizm. The horizontal lines denote median values. C = untreated CLL. B. - C. Protein levels of IAPs (XIAP, cIAP1, and cIAP2) and Bcl-2 family anti-apoptotic proteins (Bcl-2, Mcl-1, and Bcl-xL) were determined by immunoblotting. Pt 67a-d denotes that this patient arrived twice to the clinic and the immunoblot analyses were done twice. GAPDH was used as a loading control. D. Mouse embryo fibroblasts for wild-type (WT) or double-knockout (DKO) Bax/Bak were incubated without or with various concentrations of smac066 for 24 hr ( n = 3). Percent viable cells were determined by annexin/PI binding assay ( n = 3; error bars denote mean ± SEM), and percent growth inhibition was determined by the cell counting method ( n = 3; one representative data is produced). The data are expressed as percent relative to control (untreated cells). DMSO = dimethyl sulfoxide.

Techniques Used: Incubation, Binding Assay, Derivative Assay, Double Knockout, Inhibition, Cell Counting, Produced

Effect of bone marrow and lymph node microenvironments on smac066-driven apoptosis CLL lymphocytes were co-cultured with NKTert stromal cells (Str) ( A. ; n = 33) or nurse-like cells (NLC) ( B. ; n = 11) in the presence or absence of smac066 (S), (24 hr) and percent viable cells was determined by annexin/PI binding assay. The horizontal lines denote median values. The given p values are derived from paired t -test analyzed using Graph Pad Prizm. The horizontal lines denote median values. C = untreated CLL. C. Primary CLL cells were co-cultured with NKtert stromal cells, and the samples were evaluated for IAPs (XIAP and cIAP2) and anti-apoptotic proteins Bcl-2 and Mcl-1. D. - E. CLL cells were incubated with NKtert stromal cells in the presence or absence of smac066, and expression of IAPs (XIAP and cIAP2), anti-apoptotic protein Mcl-1, and apoptosis marker poly(ADP-ribose) polymerase as well as caspase cleavages (caspases 8, 9, and 3) were evaluated by immunoblotting ( n = 3). GAPDH was used as a loading control.
Figure Legend Snippet: Effect of bone marrow and lymph node microenvironments on smac066-driven apoptosis CLL lymphocytes were co-cultured with NKTert stromal cells (Str) ( A. ; n = 33) or nurse-like cells (NLC) ( B. ; n = 11) in the presence or absence of smac066 (S), (24 hr) and percent viable cells was determined by annexin/PI binding assay. The horizontal lines denote median values. The given p values are derived from paired t -test analyzed using Graph Pad Prizm. The horizontal lines denote median values. C = untreated CLL. C. Primary CLL cells were co-cultured with NKtert stromal cells, and the samples were evaluated for IAPs (XIAP and cIAP2) and anti-apoptotic proteins Bcl-2 and Mcl-1. D. - E. CLL cells were incubated with NKtert stromal cells in the presence or absence of smac066, and expression of IAPs (XIAP and cIAP2), anti-apoptotic protein Mcl-1, and apoptosis marker poly(ADP-ribose) polymerase as well as caspase cleavages (caspases 8, 9, and 3) were evaluated by immunoblotting ( n = 3). GAPDH was used as a loading control.

Techniques Used: Cell Culture, Binding Assay, Derivative Assay, Incubation, Expressing, Marker

31) Product Images from "AT-101 enhances gefitinib sensitivity in non-small cell lung cancer with EGFR T790M mutations"

Article Title: AT-101 enhances gefitinib sensitivity in non-small cell lung cancer with EGFR T790M mutations

Journal: BMC Cancer

doi: 10.1186/s12885-016-2519-3

The enhanced therapeutic effect of AT-101 on gefitinib in NSCLC cells with the T790M mutation through inhibition of antiapoptotic proteins and molecules of EGFR pathway. PC-9-GR and H1975 cells were treated with 5 μM AT-101, 1μM gefitinib or a combination as indicated for 12 hours. Western blot analysis was performed to detect the expression of p-EGFR, EGFR, p-Akt, Akt, p-Erk, Erk, Bcl-2, Bcl-xl, Mcl-1, and cleaved caspase 3. β-actin was used as the loading control
Figure Legend Snippet: The enhanced therapeutic effect of AT-101 on gefitinib in NSCLC cells with the T790M mutation through inhibition of antiapoptotic proteins and molecules of EGFR pathway. PC-9-GR and H1975 cells were treated with 5 μM AT-101, 1μM gefitinib or a combination as indicated for 12 hours. Western blot analysis was performed to detect the expression of p-EGFR, EGFR, p-Akt, Akt, p-Erk, Erk, Bcl-2, Bcl-xl, Mcl-1, and cleaved caspase 3. β-actin was used as the loading control

Techniques Used: Mutagenesis, Inhibition, Western Blot, Expressing

32) Product Images from "Simultaneous gene silencing of Bcl-2, XIAP and Survivin re-sensitizes pancreatic cancer cells towards apoptosis"

Article Title: Simultaneous gene silencing of Bcl-2, XIAP and Survivin re-sensitizes pancreatic cancer cells towards apoptosis

Journal: BMC Cancer

doi: 10.1186/1471-2407-10-379

Gene-silencing of Bcl-2, Survivin and XIAP . Western blot showed efficient silencing in transfected MiaPaCa-2 ( A ) and AsPC-1 cells ( B ). 50,000 cells/well were single-transfected with carrier solution (lane 1) and siRNA against Luciferase (lane 2) as control. SGS, lowST and ST all effectively silenced the three target genes (lane 3-5). Efficient knock-down was also shown in the lowST group by RT-PCR in MiaPaCa-2 ( C ) and AsPC-1 cells ( D ). White bars show controls, grey bars signify transfected cells. All samples were normalized to β-Actin as a house-keeping gene. SGS = Simultaneous gene silencing; lowST = Low dose siRNA transfection; ST = Standard dose siRNA transfection.
Figure Legend Snippet: Gene-silencing of Bcl-2, Survivin and XIAP . Western blot showed efficient silencing in transfected MiaPaCa-2 ( A ) and AsPC-1 cells ( B ). 50,000 cells/well were single-transfected with carrier solution (lane 1) and siRNA against Luciferase (lane 2) as control. SGS, lowST and ST all effectively silenced the three target genes (lane 3-5). Efficient knock-down was also shown in the lowST group by RT-PCR in MiaPaCa-2 ( C ) and AsPC-1 cells ( D ). White bars show controls, grey bars signify transfected cells. All samples were normalized to β-Actin as a house-keeping gene. SGS = Simultaneous gene silencing; lowST = Low dose siRNA transfection; ST = Standard dose siRNA transfection.

Techniques Used: Western Blot, Transfection, Luciferase, Reverse Transcription Polymerase Chain Reaction

33) Product Images from "GSK-3? inhibition promotes cell death, apoptosis, and in vivo tumor growth delay in neuroblastoma Neuro-2A cell line"

Article Title: GSK-3? inhibition promotes cell death, apoptosis, and in vivo tumor growth delay in neuroblastoma Neuro-2A cell line

Journal: Journal of Neuro-Oncology

doi: 10.1007/s11060-010-0491-3

GSK-3β inhibition alters the expression of anti-apoptotic proteins. GSK-3β was inhibited in Neuro-2A cells either by treating with a small molecule inhibitor of GSK-3β SB415286 (25 μM) or with a specific shRNA for GSK-3β. Western blot analysis was performed to determine the cellular protein levels of β-catenin, XAIP and Bcl-2. Actin was used to assess protein loading in each lane
Figure Legend Snippet: GSK-3β inhibition alters the expression of anti-apoptotic proteins. GSK-3β was inhibited in Neuro-2A cells either by treating with a small molecule inhibitor of GSK-3β SB415286 (25 μM) or with a specific shRNA for GSK-3β. Western blot analysis was performed to determine the cellular protein levels of β-catenin, XAIP and Bcl-2. Actin was used to assess protein loading in each lane

Techniques Used: Inhibition, Expressing, shRNA, Western Blot

34) Product Images from "Drug-Tolerant Cancer Cells Show Reduced Tumor-Initiating Capacity: Depletion of CD44+ Cells and Evidence for Epigenetic Mechanisms"

Article Title: Drug-Tolerant Cancer Cells Show Reduced Tumor-Initiating Capacity: Depletion of CD44+ Cells and Evidence for Epigenetic Mechanisms

Journal: PLoS ONE

doi: 10.1371/journal.pone.0024397

Molecular changes and reduced CD44 + cells in drug-tolerant Du145 cell cultures. A. Whole cell lysate from the cell types indicated was used in Western blotting of p21, p27, Bcl-2, and hTERT and the blot was reprobed for β-actin. NS, non-specific. B. Western blotting of CD44 and ABCG2. The blot was reprobed for β-actin and GAPDH. C–D. Du145 and drug-tolerant Du145 cells were plated on glass coverslips and stained for CD44 using monoclonal antibody. Shown are representative images (C) and quantification of CD44 + cells (D; mean ± S.D, *, P
Figure Legend Snippet: Molecular changes and reduced CD44 + cells in drug-tolerant Du145 cell cultures. A. Whole cell lysate from the cell types indicated was used in Western blotting of p21, p27, Bcl-2, and hTERT and the blot was reprobed for β-actin. NS, non-specific. B. Western blotting of CD44 and ABCG2. The blot was reprobed for β-actin and GAPDH. C–D. Du145 and drug-tolerant Du145 cells were plated on glass coverslips and stained for CD44 using monoclonal antibody. Shown are representative images (C) and quantification of CD44 + cells (D; mean ± S.D, *, P

Techniques Used: Western Blot, Staining

35) Product Images from "Protective Effect of Minocycline Against Cisplatin-induced Ototoxicity"

Article Title: Protective Effect of Minocycline Against Cisplatin-induced Ototoxicity

Journal: Clinical and Experimental Otorhinolaryngology

doi: 10.3342/ceo.2011.4.2.77

Cells pretreated with 10 µM minocycline and cultured in 4 µg/mL or 8 µg/mL cisplatin were analyzed using the Western blotting technique with antibodies targeting Bcl-2, p-JUN, cleaved caspase-3, cleaved polymerase (PARP), and AIF. Bcl-2 expression was elevated after the pretreatment with minocycline. Minocycline pretreatment decreased cisplatin-induced cleaved caspase 3 activity at the 4 µg/mL, but not the 8 µg/mL dose. The expression of p-JUN, cleaved PARP, and apoptosis-inducing factor (AIF) increased by cisplatin treatment, and suppressed by minocycline pretreatment.
Figure Legend Snippet: Cells pretreated with 10 µM minocycline and cultured in 4 µg/mL or 8 µg/mL cisplatin were analyzed using the Western blotting technique with antibodies targeting Bcl-2, p-JUN, cleaved caspase-3, cleaved polymerase (PARP), and AIF. Bcl-2 expression was elevated after the pretreatment with minocycline. Minocycline pretreatment decreased cisplatin-induced cleaved caspase 3 activity at the 4 µg/mL, but not the 8 µg/mL dose. The expression of p-JUN, cleaved PARP, and apoptosis-inducing factor (AIF) increased by cisplatin treatment, and suppressed by minocycline pretreatment.

Techniques Used: Cell Culture, Western Blot, Expressing, Activity Assay

The cisplatin-induced apoptosis pathway in House Ear Institute-Organ of Corti 1 (HEI-OC1) cells and the proposed mechanism mediating the protective effect of minocycline. The black arrow (→) indicates activation, and the blocked arrow head (→|) indicates inhibition. Our data show that minocycline activates Bcl-2 and decreases cleaved caspase-3, poly (ADP-ribose) polymerase (PARP), apoptosis-inducing factor (AIF) activity. These findings and those of previous studies suggest that minocycline activates Bcl-2 and inhibits downstream caspase-3 in the caspase-dependent pathway, and suppresses PARP-1 and downstream AIF in the caspase-independent pathway.
Figure Legend Snippet: The cisplatin-induced apoptosis pathway in House Ear Institute-Organ of Corti 1 (HEI-OC1) cells and the proposed mechanism mediating the protective effect of minocycline. The black arrow (→) indicates activation, and the blocked arrow head (→|) indicates inhibition. Our data show that minocycline activates Bcl-2 and decreases cleaved caspase-3, poly (ADP-ribose) polymerase (PARP), apoptosis-inducing factor (AIF) activity. These findings and those of previous studies suggest that minocycline activates Bcl-2 and inhibits downstream caspase-3 in the caspase-dependent pathway, and suppresses PARP-1 and downstream AIF in the caspase-independent pathway.

Techniques Used: Activation Assay, Inhibition, Activity Assay

36) Product Images from "Growth Hormone-Releaser Diet Attenuates Cognitive Dysfunction in Klotho Mutant Mice via Insulin-Like Growth Factor-1 Receptor Activation in a Genetic Aging Model"

Article Title: Growth Hormone-Releaser Diet Attenuates Cognitive Dysfunction in Klotho Mutant Mice via Insulin-Like Growth Factor-1 Receptor Activation in a Genetic Aging Model

Journal: Endocrinology and Metabolism

doi: 10.3803/EnM.2014.29.3.336

Effect of JB-1, an insulin-like growth factor-1 (IGF-1) receptor antagonist, on the growth hormone (GH)-releaser diet-mediated attenuation of changes in the expression of (A) Bax, (B) cleaved caspase-3, (C) Bcl-2, and (D) Bcl-xL in the hippocampus of klotho mutant mice. Each value is the mean±SEM of six animals. aCSF, artificial cerebrospinal fluid; Veh, vehicle diet; GHR, GH-releaser diet. a P
Figure Legend Snippet: Effect of JB-1, an insulin-like growth factor-1 (IGF-1) receptor antagonist, on the growth hormone (GH)-releaser diet-mediated attenuation of changes in the expression of (A) Bax, (B) cleaved caspase-3, (C) Bcl-2, and (D) Bcl-xL in the hippocampus of klotho mutant mice. Each value is the mean±SEM of six animals. aCSF, artificial cerebrospinal fluid; Veh, vehicle diet; GHR, GH-releaser diet. a P

Techniques Used: Expressing, Mutagenesis, Mouse Assay

37) Product Images from "Neuroprotection of a Novel Cyclopeptide C*HSDGIC* from the Cyclization of PACAP (1–5) in Cellular and Rodent Models of Retinal Ganglion Cell Apoptosis"

Article Title: Neuroprotection of a Novel Cyclopeptide C*HSDGIC* from the Cyclization of PACAP (1–5) in Cellular and Rodent Models of Retinal Ganglion Cell Apoptosis

Journal: PLoS ONE

doi: 10.1371/journal.pone.0108090

Western-blot analysis of RGC-5 cells exposed to UVB irradiation with or without the pretreatment of 10 µM CHC or 100 nM PACAP. UVB exposure caused a significant decrease in the protein level of Bcl-2 and a concomitant increase of Bax, while CHC significantly decreased the expression of apoptotic marker Bax and increased Bcl-2 expression. The results are expressed as means±S.D. (*P
Figure Legend Snippet: Western-blot analysis of RGC-5 cells exposed to UVB irradiation with or without the pretreatment of 10 µM CHC or 100 nM PACAP. UVB exposure caused a significant decrease in the protein level of Bcl-2 and a concomitant increase of Bax, while CHC significantly decreased the expression of apoptotic marker Bax and increased Bcl-2 expression. The results are expressed as means±S.D. (*P

Techniques Used: Western Blot, Irradiation, Expressing, Marker

38) Product Images from "Neuroprotection of a Novel Cyclopeptide C*HSDGIC* from the Cyclization of PACAP (1–5) in Cellular and Rodent Models of Retinal Ganglion Cell Apoptosis"

Article Title: Neuroprotection of a Novel Cyclopeptide C*HSDGIC* from the Cyclization of PACAP (1–5) in Cellular and Rodent Models of Retinal Ganglion Cell Apoptosis

Journal: PLoS ONE

doi: 10.1371/journal.pone.0108090

Western-blot analysis of RGC-5 cells exposed to UVB irradiation with or without the pretreatment of 10 µM CHC or 100 nM PACAP. UVB exposure caused a significant decrease in the protein level of Bcl-2 and a concomitant increase of Bax, while CHC significantly decreased the expression of apoptotic marker Bax and increased Bcl-2 expression. The results are expressed as means±S.D. (*P
Figure Legend Snippet: Western-blot analysis of RGC-5 cells exposed to UVB irradiation with or without the pretreatment of 10 µM CHC or 100 nM PACAP. UVB exposure caused a significant decrease in the protein level of Bcl-2 and a concomitant increase of Bax, while CHC significantly decreased the expression of apoptotic marker Bax and increased Bcl-2 expression. The results are expressed as means±S.D. (*P

Techniques Used: Western Blot, Irradiation, Expressing, Marker

39) Product Images from "Cholesterol-enriched diet causes age-related macular degeneration-like pathology in rabbit retina"

Article Title: Cholesterol-enriched diet causes age-related macular degeneration-like pathology in rabbit retina

Journal: BMC Ophthalmology

doi: 10.1186/1471-2415-11-22

Cholesterol-enriched diet caused apoptotic cell death . A . Western blot results showed a decrease in the levels of the anti-apoptotic protein Bcl-2 and an increase in levels of the pro-apoptotic protein Bax levels in the retinas of rabbits fed with cholesterol-enriched diet compared to control rabbits. B . Levels of the endoplasmic reticulum stress marker gadd153 were increased in cholesterol-fed rabbits as shown by Western blotting. C . While no TUNEL-positive cells were detected in retinas from control rabbits, a large number of TUNEL-positive cells were observed in retinas of cholesterol-fed rabbits. Propidium iodide (red) was used as a counterstain for nuclei. Bar = 20 μm. *p
Figure Legend Snippet: Cholesterol-enriched diet caused apoptotic cell death . A . Western blot results showed a decrease in the levels of the anti-apoptotic protein Bcl-2 and an increase in levels of the pro-apoptotic protein Bax levels in the retinas of rabbits fed with cholesterol-enriched diet compared to control rabbits. B . Levels of the endoplasmic reticulum stress marker gadd153 were increased in cholesterol-fed rabbits as shown by Western blotting. C . While no TUNEL-positive cells were detected in retinas from control rabbits, a large number of TUNEL-positive cells were observed in retinas of cholesterol-fed rabbits. Propidium iodide (red) was used as a counterstain for nuclei. Bar = 20 μm. *p

Techniques Used: Western Blot, Marker, TUNEL Assay

40) Product Images from "Role of dopamine D2 receptors in ischemia/reperfusion induced apoptosis of cultured neonatal rat cardiomyocytes"

Article Title: Role of dopamine D2 receptors in ischemia/reperfusion induced apoptosis of cultured neonatal rat cardiomyocytes

Journal: Journal of Biomedical Science

doi: 10.1186/1423-0127-18-18

Expression of caspase-9 (A), release of cytochrome c (B), and expression of Bcl-2 (C) determined by Western blot analysis . The intensity of each band was quantified by densitometry, and data were normalized to the β-actin signal. The expression levels in the control group were considered the basal levels, and the others are expressed as fold change from the control group. The fold change values represent the means ± S.E.M. of five determinations. ▼▼ P
Figure Legend Snippet: Expression of caspase-9 (A), release of cytochrome c (B), and expression of Bcl-2 (C) determined by Western blot analysis . The intensity of each band was quantified by densitometry, and data were normalized to the β-actin signal. The expression levels in the control group were considered the basal levels, and the others are expressed as fold change from the control group. The fold change values represent the means ± S.E.M. of five determinations. ▼▼ P

Techniques Used: Expressing, Western Blot

41) Product Images from "Oral treatment with the herbal formula B307 alleviates cardiac toxicity in doxorubicin-treated mice via suppressing oxidative stress, inflammation, and apoptosis"

Article Title: Oral treatment with the herbal formula B307 alleviates cardiac toxicity in doxorubicin-treated mice via suppressing oxidative stress, inflammation, and apoptosis

Journal: OncoTargets and therapy

doi: 10.2147/OTT.S82936

The schematic diagram illustrates that oral treatment with the herbal formula B307 alleviates cardiotoxicity in doxorubicin-treated mice via suppressing hypoxia, oxidative stress, inflammation, and apoptosis in the heart tissue. Abbreviations: eNOS, endothelial nitric oxide synthase; SOD2, superoxide dismutase 2; ROS, reactive oxygen species; 3-NT, neurotrophin-3; 4-HNE, 4-hydroxynonenal; NF-κB, nuclear factor-κB; TNF-α, tumor necrosis factor alpha; er, endoplasmic reticulum; Bcl-2, B-cell lymphoma 2; Bax, Bcl-2-associated X protein; Cyto-C, cytochrome C.
Figure Legend Snippet: The schematic diagram illustrates that oral treatment with the herbal formula B307 alleviates cardiotoxicity in doxorubicin-treated mice via suppressing hypoxia, oxidative stress, inflammation, and apoptosis in the heart tissue. Abbreviations: eNOS, endothelial nitric oxide synthase; SOD2, superoxide dismutase 2; ROS, reactive oxygen species; 3-NT, neurotrophin-3; 4-HNE, 4-hydroxynonenal; NF-κB, nuclear factor-κB; TNF-α, tumor necrosis factor alpha; er, endoplasmic reticulum; Bcl-2, B-cell lymphoma 2; Bax, Bcl-2-associated X protein; Cyto-C, cytochrome C.

Techniques Used: Mouse Assay

Cardiac levels of Bcl-2, a marker of anti-apoptosis, and Bax and Cyto-C, two markers of apoptosis, in mice under sham, B307, DOX, and B307+DOX treatments. Notes: ( A ) IHC staining illustrates that cardiac expression levels of Bcl-2 in the mice were visibly enhanced under oral B307 treatment but were visibly reduced under DOX treatment. As to the DOX-treated mice, cardiac expression levels of Bcl-2 were visibly enhanced under oral B307 treatment. On the other hand, cardiac expression levels of Bax and Cyto-C in the mice were visibly reduced under oral B307 treatment but were visibly enhanced under DOX treatment. As to the DOX-treated mice, cardiac expression levels of Bax and Cyto-C were visibly reduced under oral B307 treatment. ( B ) Western blotting analysis shows the following: (a) expression levels of cardiac Bcl-2, Bax, and Cyto-C under sham, B307, DOX, and B307+DOX treatments and (b) the quantified ratio of Bcl-2/Bax in the heart tissue of the mice was significantly increased under oral B307 treatment but were significantly reduced under DOX treatment. As to the DOX-treated mice, the quantified ratio of Bcl-2/Bax in the heart tissue was significantly increased under oral B307 treatment. On the other hand, quantified Cyto-C levels in the heart tissue of the mice were significantly decreased under oral B307 treatment but were significantly enhanced under DOX treatment. As to the DOX-treated mice, quantified Cyto-C levels in the heart tissue were significantly reduced under oral B307 treatment. The number of mice under sham, B307, DOX, and B307+DOX treatments was six for each group. Values are mean ± SEM (* P
Figure Legend Snippet: Cardiac levels of Bcl-2, a marker of anti-apoptosis, and Bax and Cyto-C, two markers of apoptosis, in mice under sham, B307, DOX, and B307+DOX treatments. Notes: ( A ) IHC staining illustrates that cardiac expression levels of Bcl-2 in the mice were visibly enhanced under oral B307 treatment but were visibly reduced under DOX treatment. As to the DOX-treated mice, cardiac expression levels of Bcl-2 were visibly enhanced under oral B307 treatment. On the other hand, cardiac expression levels of Bax and Cyto-C in the mice were visibly reduced under oral B307 treatment but were visibly enhanced under DOX treatment. As to the DOX-treated mice, cardiac expression levels of Bax and Cyto-C were visibly reduced under oral B307 treatment. ( B ) Western blotting analysis shows the following: (a) expression levels of cardiac Bcl-2, Bax, and Cyto-C under sham, B307, DOX, and B307+DOX treatments and (b) the quantified ratio of Bcl-2/Bax in the heart tissue of the mice was significantly increased under oral B307 treatment but were significantly reduced under DOX treatment. As to the DOX-treated mice, the quantified ratio of Bcl-2/Bax in the heart tissue was significantly increased under oral B307 treatment. On the other hand, quantified Cyto-C levels in the heart tissue of the mice were significantly decreased under oral B307 treatment but were significantly enhanced under DOX treatment. As to the DOX-treated mice, quantified Cyto-C levels in the heart tissue were significantly reduced under oral B307 treatment. The number of mice under sham, B307, DOX, and B307+DOX treatments was six for each group. Values are mean ± SEM (* P

Techniques Used: Marker, Mouse Assay, Immunohistochemistry, Staining, Expressing, Western Blot

42) Product Images from "Metronomic vinorelbine: Anti-angiogenic activity in vitro in normoxic and severe hypoxic conditions, and severe hypoxia-induced resistance to its anti-proliferative effect with reversal by Akt inhibition"

Article Title: Metronomic vinorelbine: Anti-angiogenic activity in vitro in normoxic and severe hypoxic conditions, and severe hypoxia-induced resistance to its anti-proliferative effect with reversal by Akt inhibition

Journal: International Journal of Oncology

doi: 10.3892/ijo.2015.3059

Bcl-2 protein downregulation by 10 nM vinorelbine (VRL) and severe hypoxia (0.1% O 2 ). (A) Representative western blotting for Bcl-2 and Bax. (B) The effect on Bcl-2 protein levels. (C) The effect on Bcl-2/Bax ratio. Results are expressed as mean fold change ± SD of three independent experiments. Error bars depict standard deviation (SD). One-way ANOVA; ns, not significant; * P
Figure Legend Snippet: Bcl-2 protein downregulation by 10 nM vinorelbine (VRL) and severe hypoxia (0.1% O 2 ). (A) Representative western blotting for Bcl-2 and Bax. (B) The effect on Bcl-2 protein levels. (C) The effect on Bcl-2/Bax ratio. Results are expressed as mean fold change ± SD of three independent experiments. Error bars depict standard deviation (SD). One-way ANOVA; ns, not significant; * P

Techniques Used: Western Blot, Standard Deviation

43) Product Images from "Psoralidin, An Herbal Molecule Inhibits PI3K Mediated Akt Signaling In Androgen Independent Prostate Cancer (AIPC) Cells"

Article Title: Psoralidin, An Herbal Molecule Inhibits PI3K Mediated Akt Signaling In Androgen Independent Prostate Cancer (AIPC) Cells

Journal: Cancer prevention research (Philadelphia, Pa.)

doi: 10.1158/1940-6207.CAPR-08-0129

Psoralidin inhibits NF-κB signaling in prosatate cancer cells via IκB pathway A . PC-3 and DU-145 cells were treated with psoralidin or vehicle control. Whole cell lysates were subjected to Western blot analysis using NIK, IKKα, IKKβ, pIKKα/β (Thr 23), IκB-α, pIκB-α and β-actin. B. PC-3 and DU-145 cells were treated either with psoralidin or vehicle control for varying time points and the cell lysates were assayed to determine nonphosphorylated IκB-α activity. C . PC-3 and DU-145 cells were treated with psoralidin or vehicle control. Whole cell lysates were subjected to Western blot analysis using Bcl-2, Bcl-xL, Bax and surviving. β-actin was used as the loading control. D PC-3/Neo and PC-3/Bcl-2 cells were treated with psoralidin or vehicle control. Whole cell lysates were subjected to Western blot analysis using Bcl-2 and β-actin. E. PC-3/Bcl-2 and PC-3/Neo were treated with various concentrations of psoralidin and apoptotic cells were scored after 24 h by TUNEL assay.
Figure Legend Snippet: Psoralidin inhibits NF-κB signaling in prosatate cancer cells via IκB pathway A . PC-3 and DU-145 cells were treated with psoralidin or vehicle control. Whole cell lysates were subjected to Western blot analysis using NIK, IKKα, IKKβ, pIKKα/β (Thr 23), IκB-α, pIκB-α and β-actin. B. PC-3 and DU-145 cells were treated either with psoralidin or vehicle control for varying time points and the cell lysates were assayed to determine nonphosphorylated IκB-α activity. C . PC-3 and DU-145 cells were treated with psoralidin or vehicle control. Whole cell lysates were subjected to Western blot analysis using Bcl-2, Bcl-xL, Bax and surviving. β-actin was used as the loading control. D PC-3/Neo and PC-3/Bcl-2 cells were treated with psoralidin or vehicle control. Whole cell lysates were subjected to Western blot analysis using Bcl-2 and β-actin. E. PC-3/Bcl-2 and PC-3/Neo were treated with various concentrations of psoralidin and apoptotic cells were scored after 24 h by TUNEL assay.

Techniques Used: Western Blot, Activity Assay, TUNEL Assay

44) Product Images from "Carboxamide derivatives induce apoptosis in the U251 glioma cell line"

Article Title: Carboxamide derivatives induce apoptosis in the U251 glioma cell line

Journal: Oncology Letters

doi: 10.3892/ol.2019.10434

Effect of carboxamide derivatives and TMZ on the expression of apoptosis-associated genes in U251 cells. (A) Caspase activity assays showed that carboxamide derivatives (N2 and S2) and TMZ induced caspase-3, −8 and −9 activity in U251 cells. (B) Western blot assays demonstrated that the carboxamide derivatives and TMZ reduced Bcl-2 and survivin protein expression levels in U251 cells. (C) Carboxamide derivatives and TMZ also reduced the mRNA expression levels of Bcl-2 and survivin in U251 cells. *P
Figure Legend Snippet: Effect of carboxamide derivatives and TMZ on the expression of apoptosis-associated genes in U251 cells. (A) Caspase activity assays showed that carboxamide derivatives (N2 and S2) and TMZ induced caspase-3, −8 and −9 activity in U251 cells. (B) Western blot assays demonstrated that the carboxamide derivatives and TMZ reduced Bcl-2 and survivin protein expression levels in U251 cells. (C) Carboxamide derivatives and TMZ also reduced the mRNA expression levels of Bcl-2 and survivin in U251 cells. *P

Techniques Used: Expressing, Activity Assay, Western Blot

45) Product Images from "Carboxamide derivatives induce apoptosis in the U251 glioma cell line"

Article Title: Carboxamide derivatives induce apoptosis in the U251 glioma cell line

Journal: Oncology Letters

doi: 10.3892/ol.2019.10434

Effect of carboxamide derivatives and TMZ on the expression of apoptosis-associated genes in U251 cells. (A) Caspase activity assays showed that carboxamide derivatives (N2 and S2) and TMZ induced caspase-3, −8 and −9 activity in U251 cells. (B) Western blot assays demonstrated that the carboxamide derivatives and TMZ reduced Bcl-2 and survivin protein expression levels in U251 cells. (C) Carboxamide derivatives and TMZ also reduced the mRNA expression levels of Bcl-2 and survivin in U251 cells. *P
Figure Legend Snippet: Effect of carboxamide derivatives and TMZ on the expression of apoptosis-associated genes in U251 cells. (A) Caspase activity assays showed that carboxamide derivatives (N2 and S2) and TMZ induced caspase-3, −8 and −9 activity in U251 cells. (B) Western blot assays demonstrated that the carboxamide derivatives and TMZ reduced Bcl-2 and survivin protein expression levels in U251 cells. (C) Carboxamide derivatives and TMZ also reduced the mRNA expression levels of Bcl-2 and survivin in U251 cells. *P

Techniques Used: Expressing, Activity Assay, Western Blot

46) Product Images from "17β-estradiol and tamoxifen protect mice from manganese-induced dopaminergic neurotoxicity"

Article Title: 17β-estradiol and tamoxifen protect mice from manganese-induced dopaminergic neurotoxicity

Journal: Neurotoxicology

doi: 10.1016/j.neuro.2017.11.008

Effects of E2 and TX on Mn-induced apoptosis in the mouse brain. At the end of treatment with Mn, E2, and TX, tissue samples were prepared from the mouse brain as described in the Methods section. Tissues were analyzed for pro-apoptotic Bax and antiapoptotic Bcl-2 protein (A) , and the levels of Bax/Bcl-2 ratio (B) . β-actin was used as a loading control. ### , p
Figure Legend Snippet: Effects of E2 and TX on Mn-induced apoptosis in the mouse brain. At the end of treatment with Mn, E2, and TX, tissue samples were prepared from the mouse brain as described in the Methods section. Tissues were analyzed for pro-apoptotic Bax and antiapoptotic Bcl-2 protein (A) , and the levels of Bax/Bcl-2 ratio (B) . β-actin was used as a loading control. ### , p

Techniques Used:

47) Product Images from "Melatonin Treatment Regulates SIRT3 Expression in Early Brain Injury (EBI) Due to Reactive Oxygen Species (ROS) in a Mouse Model of Subarachnoid Hemorrhage (SAH)"

Article Title: Melatonin Treatment Regulates SIRT3 Expression in Early Brain Injury (EBI) Due to Reactive Oxygen Species (ROS) in a Mouse Model of Subarachnoid Hemorrhage (SAH)

Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

doi: 10.12659/MSM.907734

Melatonin was associated with early brain injury (EBI) after subarachnoid hemorrhage (SAH) by affecting redox and apoptotic genes. Three mouse groups were studied: the subarachnoid hemorrhage (SAH) group; the sham group; and the SAH + melatonin-treated group (intraperitoneal dose, 150 mg/kg). ( A ) Melatonin treatment increased Bcl-2 and Sirt3 protein levels, and decreased SOD2, Bax, and cleaved caspase-3 levels following SAH. ( B ) Sirt3 protein levels in the SAH group and SAH + melatonin-treatment group were much lower than in the sham group. ( C ) SOD2 levels in the SAH + melatonin-treatment group were much greater than in the sham group, and the SAH group. ( D ) Bax levels in the SAH group were much greater than in the SAH + melatonin-treatment group, and both of them were much greater than in the sham group. ( E ) Bcl-2 levels in the SAH and SAH + melatonin-treated groups were significantly lower than in the sham group. ( F ) Cleaved caspase-3 levels in the SAH + melatonin-treatment group were significantly greater than in the sham group, and were significantly greater than in the SAH group.
Figure Legend Snippet: Melatonin was associated with early brain injury (EBI) after subarachnoid hemorrhage (SAH) by affecting redox and apoptotic genes. Three mouse groups were studied: the subarachnoid hemorrhage (SAH) group; the sham group; and the SAH + melatonin-treated group (intraperitoneal dose, 150 mg/kg). ( A ) Melatonin treatment increased Bcl-2 and Sirt3 protein levels, and decreased SOD2, Bax, and cleaved caspase-3 levels following SAH. ( B ) Sirt3 protein levels in the SAH group and SAH + melatonin-treatment group were much lower than in the sham group. ( C ) SOD2 levels in the SAH + melatonin-treatment group were much greater than in the sham group, and the SAH group. ( D ) Bax levels in the SAH group were much greater than in the SAH + melatonin-treatment group, and both of them were much greater than in the sham group. ( E ) Bcl-2 levels in the SAH and SAH + melatonin-treated groups were significantly lower than in the sham group. ( F ) Cleaved caspase-3 levels in the SAH + melatonin-treatment group were significantly greater than in the sham group, and were significantly greater than in the SAH group.

Techniques Used:

48) Product Images from "Astragalus polysaccharides suppress ICAM-1 and VCAM-1 expression in TNF-α-treated human vascular endothelial cells by blocking NF-κB activation"

Article Title: Astragalus polysaccharides suppress ICAM-1 and VCAM-1 expression in TNF-α-treated human vascular endothelial cells by blocking NF-κB activation

Journal: Acta Pharmacologica Sinica

doi: 10.1038/aps.2013.46

APS down-regulate the expression of adhesion molecules by inhibition of NF-κB activation. (A) Western blotting analysis of ICAM-1, VCAM-1, pIκBα, IκBα, pNF-κB, NF-κB, Bax, and Bcl-2 abundance in
Figure Legend Snippet: APS down-regulate the expression of adhesion molecules by inhibition of NF-κB activation. (A) Western blotting analysis of ICAM-1, VCAM-1, pIκBα, IκBα, pNF-κB, NF-κB, Bax, and Bcl-2 abundance in

Techniques Used: Expressing, Inhibition, Activation Assay, Western Blot

49) Product Images from "JARID1B deletion induced apoptosis in Jeko-1 and HL-60 cell lines"

Article Title: JARID1B deletion induced apoptosis in Jeko-1 and HL-60 cell lines

Journal: International Journal of Clinical and Experimental Pathology

doi:

siRNA JARID1B-induced apoptosis was mitochondria-mediated and caspase dependent. Jeko-1 and HL-60 cells were treated respectively for 24 hours with siRNA JARID1B in 0, 30, 60, 120 nmol/L. After siRNA JARID1B treatment, cytosolic proteins were isolated and separated in 12% SDS gel, transferred onto PVDF membrane and blotted with BCL-2, procaspase-3, C-myc antibodys. The proteins were determined by immunoblotting using appropriate antibody. β-actin was used as a loading control. A siRNA JARID1B breakup BCL-2, pro-caspase-3 and C-myc significantly in Jeko-1 cell. B siRNA JARID1B breakup BCL-2, pro-caspase-3 and C-myc in HL-60 cell.
Figure Legend Snippet: siRNA JARID1B-induced apoptosis was mitochondria-mediated and caspase dependent. Jeko-1 and HL-60 cells were treated respectively for 24 hours with siRNA JARID1B in 0, 30, 60, 120 nmol/L. After siRNA JARID1B treatment, cytosolic proteins were isolated and separated in 12% SDS gel, transferred onto PVDF membrane and blotted with BCL-2, procaspase-3, C-myc antibodys. The proteins were determined by immunoblotting using appropriate antibody. β-actin was used as a loading control. A siRNA JARID1B breakup BCL-2, pro-caspase-3 and C-myc significantly in Jeko-1 cell. B siRNA JARID1B breakup BCL-2, pro-caspase-3 and C-myc in HL-60 cell.

Techniques Used: Isolation, SDS-Gel

50) Product Images from "Changes in Caspase-3, B Cell Leukemia/Lymphoma-2, Interleukin-6, Tumor Necrosis Factor-α and Vascular Endothelial Growth Factor Gene Expression after Human Umbilical Cord Blood Derived Mesenchymal Stem Cells Transfusion in Pulmonary Hypertension Rat Models"

Article Title: Changes in Caspase-3, B Cell Leukemia/Lymphoma-2, Interleukin-6, Tumor Necrosis Factor-α and Vascular Endothelial Growth Factor Gene Expression after Human Umbilical Cord Blood Derived Mesenchymal Stem Cells Transfusion in Pulmonary Hypertension Rat Models

Journal: Korean Circulation Journal

doi: 10.4070/kcj.2016.46.1.79

Changes of caspase-3 (A), Bcl-2 (B), VEGF (C), IL-6 (D), TNF-α (E), and BNP (F) protein expression levels after hUCB-MSCs injection in PAH rat heart tissues. The protein expressions of caspase-3, Bcl-2 and TNF-α were greatly decreased in the U group, as compared with the M group at week 2. The protein expressions of VEGF, IL-6 and BNP were significantly decreased in the U group in comparison with the M group at weeks 2 and 4 (p
Figure Legend Snippet: Changes of caspase-3 (A), Bcl-2 (B), VEGF (C), IL-6 (D), TNF-α (E), and BNP (F) protein expression levels after hUCB-MSCs injection in PAH rat heart tissues. The protein expressions of caspase-3, Bcl-2 and TNF-α were greatly decreased in the U group, as compared with the M group at week 2. The protein expressions of VEGF, IL-6 and BNP were significantly decreased in the U group in comparison with the M group at weeks 2 and 4 (p

Techniques Used: Expressing, Injection

Changes in caspase-3, Bcl-2, IL-6, TNF-α and VEGF protein expression levels after hUCB-MSCs injection in PAH rat lung tissues. The protein expression levels of caspase-3 (A), Bcl-2 (B), VEGF (C), IL-6 (D) and TNF-α (E) were significantly increased in the M group, as compared with the C group at weeks 2 and 4. The protein expression levels of caspase-3, Bcl-2, IL-6 and VEGF were greatly decreased in the M group, as compared with the C group at week 4. * p
Figure Legend Snippet: Changes in caspase-3, Bcl-2, IL-6, TNF-α and VEGF protein expression levels after hUCB-MSCs injection in PAH rat lung tissues. The protein expression levels of caspase-3 (A), Bcl-2 (B), VEGF (C), IL-6 (D) and TNF-α (E) were significantly increased in the M group, as compared with the C group at weeks 2 and 4. The protein expression levels of caspase-3, Bcl-2, IL-6 and VEGF were greatly decreased in the M group, as compared with the C group at week 4. * p

Techniques Used: Expressing, Injection

Immunohistochemical staing in the lung tissues. Immunohistochemical staining showed that caspase-3, Bcl-2, IL-6, TNF-α and VEGF expression levels were significantly higher in the M group than in the C group; however, the e xpression was lower in the U group than in the M group. * p
Figure Legend Snippet: Immunohistochemical staing in the lung tissues. Immunohistochemical staining showed that caspase-3, Bcl-2, IL-6, TNF-α and VEGF expression levels were significantly higher in the M group than in the C group; however, the e xpression was lower in the U group than in the M group. * p

Techniques Used: Immunohistochemistry, Staining, Expressing

Changes in caspase-3, Bcl-2, IL-6, TNF-α and VEGF mRNA expression levels after hUCB-MSCs injection in PAH rat lung tissues. The mRNA levels of caspase-3 (A), Bcl-2 (B), VEGF (C), IL-6 (D) and TNF-α (E) were significantly increased in the M group in comparison with the C group at weeks 2 and 4. The mRNA levels of caspase-3, Bcl-2, VEGF, IL-6 and TNF-α were greatly decreased in the U group, as compared with the M group at week 4. * p
Figure Legend Snippet: Changes in caspase-3, Bcl-2, IL-6, TNF-α and VEGF mRNA expression levels after hUCB-MSCs injection in PAH rat lung tissues. The mRNA levels of caspase-3 (A), Bcl-2 (B), VEGF (C), IL-6 (D) and TNF-α (E) were significantly increased in the M group in comparison with the C group at weeks 2 and 4. The mRNA levels of caspase-3, Bcl-2, VEGF, IL-6 and TNF-α were greatly decreased in the U group, as compared with the M group at week 4. * p

Techniques Used: Expressing, Injection

51) Product Images from "Phosphodiesterase Type 5 (PDE5) Inhibitors Sensitize Topoisomerase II Inhibitors in Killing Prostate Cancer Through PDE5-Independent Impairment of HR and NHEJ DNA Repair Systems"

Article Title: Phosphodiesterase Type 5 (PDE5) Inhibitors Sensitize Topoisomerase II Inhibitors in Killing Prostate Cancer Through PDE5-Independent Impairment of HR and NHEJ DNA Repair Systems

Journal: Frontiers in Oncology

doi: 10.3389/fonc.2018.00681

Schematic figure for sildenafil-mediated apoptotic sensitization pathways. Doxorubicin induces cell apoptosis, which is associated with DNA repair processing composed of both HR and NHEJ repair pathways. Sildenafil results in impairment of both repair systems that are evident by Rad51 down-regulation and its decreased foci formation in the nucleus in HR pathway, and a decrease of the DNA end-binding of Ku80 in NHEJ pathway. The combination treatment ultimately causes an enhanced decrease of anti-apoptotic Bcl-2 family members, leading to the activation of caspase cascades and cell apoptosis.
Figure Legend Snippet: Schematic figure for sildenafil-mediated apoptotic sensitization pathways. Doxorubicin induces cell apoptosis, which is associated with DNA repair processing composed of both HR and NHEJ repair pathways. Sildenafil results in impairment of both repair systems that are evident by Rad51 down-regulation and its decreased foci formation in the nucleus in HR pathway, and a decrease of the DNA end-binding of Ku80 in NHEJ pathway. The combination treatment ultimately causes an enhanced decrease of anti-apoptotic Bcl-2 family members, leading to the activation of caspase cascades and cell apoptosis.

Techniques Used: Non-Homologous End Joining, Binding Assay, Activation Assay

Effect of doxorubicin and sildenafil on the expressions of Bcl-2 family members and caspases. PC-3 cells were incubated in the absence or presence of doxorubicin (1 μM) and/or sildenafil (10 μM) for 24 h. After the treatment, the cells were harvested and lysed for the detection of protein expressions of Bcl-2 family members (A) and caspases (B) by Western blot analysis. The expression was quantified using the computerized image analysis system Image J software. Data are expressed as mean ± SEM of three to five independent experiments.
Figure Legend Snippet: Effect of doxorubicin and sildenafil on the expressions of Bcl-2 family members and caspases. PC-3 cells were incubated in the absence or presence of doxorubicin (1 μM) and/or sildenafil (10 μM) for 24 h. After the treatment, the cells were harvested and lysed for the detection of protein expressions of Bcl-2 family members (A) and caspases (B) by Western blot analysis. The expression was quantified using the computerized image analysis system Image J software. Data are expressed as mean ± SEM of three to five independent experiments.

Techniques Used: Incubation, Western Blot, Expressing, Software

52) Product Images from "Dihydroartemisinin and its derivative induce apoptosis in acute myeloid leukemia through Noxa-mediated pathway requiring iron and endoperoxide moiety"

Article Title: Dihydroartemisinin and its derivative induce apoptosis in acute myeloid leukemia through Noxa-mediated pathway requiring iron and endoperoxide moiety

Journal: Oncotarget

doi:

The combined effects of DHA/X-11 with ABT-737 in HL-60 cells which overexpress Bcl-2 HL-60/neo cells, (transfected with an empty vector), and HL-60/Bcl2, (transfected with a Bcl-2 expression vector), were treated with either DHA and X-11 alone or in combination with ABT-737 for 24 h. Percentages of apoptotic cells were determined using FACS after staining with PI (A) and the apoptosis related proteins were measured by Western blot analysis (B).
Figure Legend Snippet: The combined effects of DHA/X-11 with ABT-737 in HL-60 cells which overexpress Bcl-2 HL-60/neo cells, (transfected with an empty vector), and HL-60/Bcl2, (transfected with a Bcl-2 expression vector), were treated with either DHA and X-11 alone or in combination with ABT-737 for 24 h. Percentages of apoptotic cells were determined using FACS after staining with PI (A) and the apoptosis related proteins were measured by Western blot analysis (B).

Techniques Used: Transfection, Plasmid Preparation, Expressing, FACS, Staining, Western Blot

A working model of DHA and X-11 apoptosis induction in AML cells DHA or X-11 interacts with iron to produce ROS (O 2 − ) through the endoperoxide moiety, which strongly upregulates Noxa and weakly upregulates Bim. The induced Noxa protein binds to Mcl-1 and then leads to Bak activation. The anti-apoptotic effect of Bcl-2 is antagonized by basal and induced levels of Bim. ABT-737 combined with DHA synergistically induces apoptosis in AML cells due to respective inhibition of Bcl-2/Bcl-xL and Mcl-1.
Figure Legend Snippet: A working model of DHA and X-11 apoptosis induction in AML cells DHA or X-11 interacts with iron to produce ROS (O 2 − ) through the endoperoxide moiety, which strongly upregulates Noxa and weakly upregulates Bim. The induced Noxa protein binds to Mcl-1 and then leads to Bak activation. The anti-apoptotic effect of Bcl-2 is antagonized by basal and induced levels of Bim. ABT-737 combined with DHA synergistically induces apoptosis in AML cells due to respective inhibition of Bcl-2/Bcl-xL and Mcl-1.

Techniques Used: Activation Assay, Inhibition

53) Product Images from "Para amino benzoic acid-derived self-assembled biocompatible nanoparticles for efficient delivery of siRNA"

Article Title: Para amino benzoic acid-derived self-assembled biocompatible nanoparticles for efficient delivery of siRNA

Journal: International Journal of Nanomedicine

doi: 10.2147/IJN.S86238

( A ) Real-time polymerase chain reaction analysis and ( B ) representative Western blot analysis of the Bcl-2 gene expression in HeLa cells after transfection with NP-Bcl-2-siRNA. ( C ) Densitometry graph demonstrating Bcl-2 protein expression in HeLa cells post transfection with NP-Bcl-2-siRNA. Untreated and transfected with non-silencing siRNA serves as controls. Cells transfected with Lipofectamine 2000 served as the positive control. Data represented in the graph are expressed as a ratio to the control. All the data are normalized to the house-keeping gene β-actin. Notes: Values are mean ± standard deviation; n=3; *** P
Figure Legend Snippet: ( A ) Real-time polymerase chain reaction analysis and ( B ) representative Western blot analysis of the Bcl-2 gene expression in HeLa cells after transfection with NP-Bcl-2-siRNA. ( C ) Densitometry graph demonstrating Bcl-2 protein expression in HeLa cells post transfection with NP-Bcl-2-siRNA. Untreated and transfected with non-silencing siRNA serves as controls. Cells transfected with Lipofectamine 2000 served as the positive control. Data represented in the graph are expressed as a ratio to the control. All the data are normalized to the house-keeping gene β-actin. Notes: Values are mean ± standard deviation; n=3; *** P

Techniques Used: Real-time Polymerase Chain Reaction, Western Blot, Expressing, Transfection, Positive Control, Standard Deviation

54) Product Images from "Inhibition of IkB kinase and NF-kB by a novel synthetic compound SK 2009"

Article Title: Inhibition of IkB kinase and NF-kB by a novel synthetic compound SK 2009

Journal: Bioorganic & medicinal chemistry

doi: 10.1016/j.bmc.2009.10.065

SK2009 suppresses the expression of TNF-induced cyclin D1, Bcl-2, and VEGF. KBM-5 cells (1×10 6 /mL) were co- incubated with SK2009 at 100 μM concentration along with 1 nM TNF for the indicated times. Whole-cell extracts were prepared and fractionated using 10%vSDS-PAGE, and electro-transferred to a nitrocellulose membrane and analyzed by Western blotting using antibodies specific for the individual proteins. Data is the average of 3 independent experiments.
Figure Legend Snippet: SK2009 suppresses the expression of TNF-induced cyclin D1, Bcl-2, and VEGF. KBM-5 cells (1×10 6 /mL) were co- incubated with SK2009 at 100 μM concentration along with 1 nM TNF for the indicated times. Whole-cell extracts were prepared and fractionated using 10%vSDS-PAGE, and electro-transferred to a nitrocellulose membrane and analyzed by Western blotting using antibodies specific for the individual proteins. Data is the average of 3 independent experiments.

Techniques Used: Expressing, Incubation, Concentration Assay, Polyacrylamide Gel Electrophoresis, Western Blot

55) Product Images from "Molecular mechanisms underlying the antitumor activity of (E)-N-hydroxy-3-(1-(4-methoxyphenylsulfonyl)-1,2,3,4-tetrahydroquinolin-6-yl)acrylamide in human colorectal cancer cells in vitro and in vivo"

Article Title: Molecular mechanisms underlying the antitumor activity of (E)-N-hydroxy-3-(1-(4-methoxyphenylsulfonyl)-1,2,3,4-tetrahydroquinolin-6-yl)acrylamide in human colorectal cancer cells in vitro and in vivo

Journal: Oncotarget

doi:

Effects of compound 11 on Bcl-2 family proteins and survival signaling HCT116 cells were exposed to compound 11 (0.6 μM) for the indicated times, and cell lysates were subjected to Western blot analysis using the indicated antibodies against Bcl-2 family proteins A. and members of survival signaling pathways B. GAPDH servered as a loading control.
Figure Legend Snippet: Effects of compound 11 on Bcl-2 family proteins and survival signaling HCT116 cells were exposed to compound 11 (0.6 μM) for the indicated times, and cell lysates were subjected to Western blot analysis using the indicated antibodies against Bcl-2 family proteins A. and members of survival signaling pathways B. GAPDH servered as a loading control.

Techniques Used: Western Blot

56) Product Images from "Autophagic Signaling and Proteolytic Enzyme Activity in Cardiac and Skeletal Muscle of Spontaneously Hypertensive Rats following Chronic Aerobic Exercise"

Article Title: Autophagic Signaling and Proteolytic Enzyme Activity in Cardiac and Skeletal Muscle of Spontaneously Hypertensive Rats following Chronic Aerobic Exercise

Journal: PLoS ONE

doi: 10.1371/journal.pone.0119382

Expression of mRNA and proteins involved in autophagy regulation and induction in muscle of sedentary and exercise-trained normotensive and hypertensive rats. A : quantitative analysis of Beclin-1 mRNA in WG and LV. B : representative immunoblots and quantitative analysis of Beclin-1, BNIP3, and Bcl-xL protein in WG and LV. C : representative immunoblots and quantitative analysis of Bcl-2 and p-Bcl-2 (Ser 87 ) protein in WG and LV (calculated p-Bcl-2:Bcl-2 ratio is also shown). Portions of Ponceau stained membranes are also shown to verify equal loading and quality of transfer. Values are means ± SEM ( n = 9–12). ‡ p
Figure Legend Snippet: Expression of mRNA and proteins involved in autophagy regulation and induction in muscle of sedentary and exercise-trained normotensive and hypertensive rats. A : quantitative analysis of Beclin-1 mRNA in WG and LV. B : representative immunoblots and quantitative analysis of Beclin-1, BNIP3, and Bcl-xL protein in WG and LV. C : representative immunoblots and quantitative analysis of Bcl-2 and p-Bcl-2 (Ser 87 ) protein in WG and LV (calculated p-Bcl-2:Bcl-2 ratio is also shown). Portions of Ponceau stained membranes are also shown to verify equal loading and quality of transfer. Values are means ± SEM ( n = 9–12). ‡ p

Techniques Used: Expressing, Western Blot, Staining

57) Product Images from "Apoptosis Activity of the Mouse Macrophage Cell Line J774A.1 Infected with a Recombinant BCG consisting the C-Terminus of Merozoite Surface Protein-1 of Plasmodium falciparum"

Article Title: Apoptosis Activity of the Mouse Macrophage Cell Line J774A.1 Infected with a Recombinant BCG consisting the C-Terminus of Merozoite Surface Protein-1 of Plasmodium falciparum

Journal: Tropical Life Sciences Research

doi: 10.21315/tlsr2018.29.2.5

(A) Representative result of Bcl-2 and β–actin protein expression; (B) The relative density of Bcl-2/β-actin protein expression in mouse macrophage cell line J774A.1 infected with BCG or BCG-MSP1C clones for 48 h. The untreated cells and LPS-stimulated cells were used as a negative control and positive control respectively. The data are expressed as the mean relative density of Bcl-2/β-actin protein expression ± SEM of three independent experiments. The data were analysed using RM ANOVA and * p
Figure Legend Snippet: (A) Representative result of Bcl-2 and β–actin protein expression; (B) The relative density of Bcl-2/β-actin protein expression in mouse macrophage cell line J774A.1 infected with BCG or BCG-MSP1C clones for 48 h. The untreated cells and LPS-stimulated cells were used as a negative control and positive control respectively. The data are expressed as the mean relative density of Bcl-2/β-actin protein expression ± SEM of three independent experiments. The data were analysed using RM ANOVA and * p

Techniques Used: Expressing, Infection, Clone Assay, Negative Control, Positive Control

58) Product Images from "Functional role of the nicotinic arm of the acetylcholine regulatory axis in human B-cell lines"

Article Title: Functional role of the nicotinic arm of the acetylcholine regulatory axis in human B-cell lines

Journal: Journal of Experimental Pharmacology

doi:

Nicotinic effects on pansorbin-induced activation of Daudi cells. Daudi cells, 3 × 10 6 cells/well, were incubated for 16 hours in a humid, 5% CO 2 incubator in the culture medium containing 0.05% pansorbin (Ps) in the absence or presence of 1 μM epibatidine (Epi) ± 50 μM Mec or 100 nM MLA, after which the expression of the genes encoding Cox-2, Bcl-2, and Bax at the mRNA and protein levels was measured by qPCR and ICW, respectively, as detailed in Materials and methods. The results are expressed as fold of control values determined in intact Daudi cells taken as 1. Notes: * P
Figure Legend Snippet: Nicotinic effects on pansorbin-induced activation of Daudi cells. Daudi cells, 3 × 10 6 cells/well, were incubated for 16 hours in a humid, 5% CO 2 incubator in the culture medium containing 0.05% pansorbin (Ps) in the absence or presence of 1 μM epibatidine (Epi) ± 50 μM Mec or 100 nM MLA, after which the expression of the genes encoding Cox-2, Bcl-2, and Bax at the mRNA and protein levels was measured by qPCR and ICW, respectively, as detailed in Materials and methods. The results are expressed as fold of control values determined in intact Daudi cells taken as 1. Notes: * P

Techniques Used: Activation Assay, Incubation, Expressing, Real-time Polymerase Chain Reaction

59) Product Images from "Metformin induces apoptosis of human hepatocellular carcinoma HepG2 cells by activating an AMPK/p53/miR-23a/FOXA1 pathway"

Article Title: Metformin induces apoptosis of human hepatocellular carcinoma HepG2 cells by activating an AMPK/p53/miR-23a/FOXA1 pathway

Journal: OncoTargets and therapy

doi: 10.2147/OTT.S99770

Metformin induces apoptosis in HepG2 cells. Notes: ( A ) The effect of various doses of metformin (Met) on cell viability. Cells were treated with metformin for 72 hours, and the cell viability was measured by MTT assay. ( B ) The effect of metformin on PARP cleavage and BAX and BCL-2 expression under metformin treatment. The protein expression was determined by Western blot analysis; the band density was statistically shown in the histogram in ( C ), ( D ), and ( E ). * P
Figure Legend Snippet: Metformin induces apoptosis in HepG2 cells. Notes: ( A ) The effect of various doses of metformin (Met) on cell viability. Cells were treated with metformin for 72 hours, and the cell viability was measured by MTT assay. ( B ) The effect of metformin on PARP cleavage and BAX and BCL-2 expression under metformin treatment. The protein expression was determined by Western blot analysis; the band density was statistically shown in the histogram in ( C ), ( D ), and ( E ). * P

Techniques Used: MTT Assay, Expressing, Western Blot

60) Product Images from "Luteolin Limits Infarct Size and Improves Cardiac Function after Myocardium Ischemia/Reperfusion Injury in Diabetic Rats"

Article Title: Luteolin Limits Infarct Size and Improves Cardiac Function after Myocardium Ischemia/Reperfusion Injury in Diabetic Rats

Journal: PLoS ONE

doi: 10.1371/journal.pone.0033491

Western blot analysis. Western blot analysis revealed that Luteolin treatment increased the expression of antiapoptotic proteins FGFR2 and LIF as compared with the I/R group and wortmannin group (a, b). Luteolin also enhanced phosphorylation of Akt and BAD, increased Bax expression while decreased Bcl-2 expression resulted in decreased Bax/Bcl-2 ratio in cardiac tissue that were exposed to I/R injury (c, d, e). The PI3K inhibitor wortmannin abolished the effects of Luteolin on antiapoptotic proteins expression. The columns and errors bars represent means and SD. * p
Figure Legend Snippet: Western blot analysis. Western blot analysis revealed that Luteolin treatment increased the expression of antiapoptotic proteins FGFR2 and LIF as compared with the I/R group and wortmannin group (a, b). Luteolin also enhanced phosphorylation of Akt and BAD, increased Bax expression while decreased Bcl-2 expression resulted in decreased Bax/Bcl-2 ratio in cardiac tissue that were exposed to I/R injury (c, d, e). The PI3K inhibitor wortmannin abolished the effects of Luteolin on antiapoptotic proteins expression. The columns and errors bars represent means and SD. * p

Techniques Used: Western Blot, Expressing

61) Product Images from "Phenylethyl isothiocyanate reverses cisplatin resistance in biliary tract cancer cells via glutathionylation-dependent degradation of Mcl-1"

Article Title: Phenylethyl isothiocyanate reverses cisplatin resistance in biliary tract cancer cells via glutathionylation-dependent degradation of Mcl-1

Journal: Oncotarget

doi: 10.18632/oncotarget.7171

CDDP resistance is partially associated with Mcl-1 in GBC-SD and SP cells ( A ) Immunoblot analysis of Mcl-1, Bcl-xl and Bcl-2 protein in GBC-SD cells. Left panel, cells were treated with the indicated concentrations of CDDP for 18 hrs. Right panel, cells were treated with 4 ug/ml CDDP and harvested at the indicated times. Δ-Actin was used as a loading control. ( B ) Cells were transfected with non-specific siRNA (NC) or Mcl-1 siRNA (SiMcl1) for 48 hrs and reduction in Mcl-1 was analysed by western blot ( C ) Apoptosis analysis using Annexin V/PI flow cytometry in GBC-SD cells transfected with Mcl-1 siRNA after treatment with CDDP for 24 hrs. Data shown is average of three independent experiments. * P
Figure Legend Snippet: CDDP resistance is partially associated with Mcl-1 in GBC-SD and SP cells ( A ) Immunoblot analysis of Mcl-1, Bcl-xl and Bcl-2 protein in GBC-SD cells. Left panel, cells were treated with the indicated concentrations of CDDP for 18 hrs. Right panel, cells were treated with 4 ug/ml CDDP and harvested at the indicated times. Δ-Actin was used as a loading control. ( B ) Cells were transfected with non-specific siRNA (NC) or Mcl-1 siRNA (SiMcl1) for 48 hrs and reduction in Mcl-1 was analysed by western blot ( C ) Apoptosis analysis using Annexin V/PI flow cytometry in GBC-SD cells transfected with Mcl-1 siRNA after treatment with CDDP for 24 hrs. Data shown is average of three independent experiments. * P

Techniques Used: Transfection, Western Blot, Flow Cytometry, Cytometry

62) Product Images from "Molecular Mechanisms of Melatonin Protection from Gastric Mucosal Apoptotic Injury in Experimental Burns"

Article Title: Molecular Mechanisms of Melatonin Protection from Gastric Mucosal Apoptotic Injury in Experimental Burns

Journal: Molecules : A Journal of Synthetic Chemistry and Natural Product Chemistry

doi: 10.3390/molecules23040749

Melatonin effect on Bcl-2 expression. Immunohistochemical detection of Bcl-2 in gastric mucosa. Controls ( A ); burned rats ( B ); burned melatonin-treated rats ( C ). The antigen site appears as a brown color. Representative images. Original magnification, 400×. Score index of Bcl-2 positive immunostained cells ( D ). Results are given as box plot, with median, 25th- and 75th-percentile values, and min and max values. *** p
Figure Legend Snippet: Melatonin effect on Bcl-2 expression. Immunohistochemical detection of Bcl-2 in gastric mucosa. Controls ( A ); burned rats ( B ); burned melatonin-treated rats ( C ). The antigen site appears as a brown color. Representative images. Original magnification, 400×. Score index of Bcl-2 positive immunostained cells ( D ). Results are given as box plot, with median, 25th- and 75th-percentile values, and min and max values. *** p

Techniques Used: Expressing, Immunohistochemistry

Melatonin effect on the Bax/Bcl-2 ratio (intensity index) in gastric mucosa. Results are given as means ±SEM. * p
Figure Legend Snippet: Melatonin effect on the Bax/Bcl-2 ratio (intensity index) in gastric mucosa. Results are given as means ±SEM. * p

Techniques Used:

63) Product Images from "γ-Tocotrienol Inhibits Proliferation and Induces Apoptosis via the Mitochondrial Pathway in Human Cervical Cancer HeLa Cells"

Article Title: γ-Tocotrienol Inhibits Proliferation and Induces Apoptosis via the Mitochondrial Pathway in Human Cervical Cancer HeLa Cells

Journal: Molecules : A Journal of Synthetic Chemistry and Natural Product Chemistry

doi: 10.3390/molecules22081299

Effects of γ-tocotrienol on expression of bcl-2/bax ( A ), Caspase-3 ( B ), PARP-1 ( C ), and Caspase-8 ( D ) in HeLa cells. Cells were treated with various concentrations of γ-tocotrienol for 24 h. The expression levels of the proteins were analyzed through Western blot method. * p
Figure Legend Snippet: Effects of γ-tocotrienol on expression of bcl-2/bax ( A ), Caspase-3 ( B ), PARP-1 ( C ), and Caspase-8 ( D ) in HeLa cells. Cells were treated with various concentrations of γ-tocotrienol for 24 h. The expression levels of the proteins were analyzed through Western blot method. * p

Techniques Used: Expressing, Western Blot

Effect of γ-tocotrienol on expression of proliferation and apoptosis-related proteins in HeLa cells. Cells were treated with various concentrations of γ-tocotrienol for 24 h. The expression levels of PCNA and Ki-67 ( A ), Bcl-2 and Bax ( B ) were analyzed by Western blot method. * p
Figure Legend Snippet: Effect of γ-tocotrienol on expression of proliferation and apoptosis-related proteins in HeLa cells. Cells were treated with various concentrations of γ-tocotrienol for 24 h. The expression levels of PCNA and Ki-67 ( A ), Bcl-2 and Bax ( B ) were analyzed by Western blot method. * p

Techniques Used: Expressing, Western Blot

64) Product Images from "Sensitization of estrogen receptor-positive breast cancer cell lines to 4-hydroxytamoxifen by isothiocyanates present in cruciferous plants"

Article Title: Sensitization of estrogen receptor-positive breast cancer cell lines to 4-hydroxytamoxifen by isothiocyanates present in cruciferous plants

Journal: European Journal of Nutrition

doi: 10.1007/s00394-015-0930-1

Effect of co-treatment of breast cancer cell lines with 4-hydroxytamoxifen and erucin on PARP cleavage, levels of Bcl-2, Bax, survivin and ADRP. T47D ( a ) and MCF-7 ( b ) cells were treated with 5 μM erucin (ERN) and/or 0.5 μM 4-hydroxytamoxifen (4-OH-T). BT-474 ( c ) cells were treated with 5 μM erucin (ERN) and/or 1 μM 4-hydroxytamoxifen (4-OH-T). Blots were stripped and reprobed with anti-β-actin antibody to ensure equal protein loading. Results are plotted as mean ± SE from 3 independent experiments, *significantly different compared with single agent-treated samples or **significantly different compared with one of the single agent-treated samples by one-way ANOVA followed by Bonferroni’s multiple comparison test. Data for PARP refer to the faster migrating band marked as * and are given relative to samples treated with ERN alone. Blots shown are representative of at least three independent experiments
Figure Legend Snippet: Effect of co-treatment of breast cancer cell lines with 4-hydroxytamoxifen and erucin on PARP cleavage, levels of Bcl-2, Bax, survivin and ADRP. T47D ( a ) and MCF-7 ( b ) cells were treated with 5 μM erucin (ERN) and/or 0.5 μM 4-hydroxytamoxifen (4-OH-T). BT-474 ( c ) cells were treated with 5 μM erucin (ERN) and/or 1 μM 4-hydroxytamoxifen (4-OH-T). Blots were stripped and reprobed with anti-β-actin antibody to ensure equal protein loading. Results are plotted as mean ± SE from 3 independent experiments, *significantly different compared with single agent-treated samples or **significantly different compared with one of the single agent-treated samples by one-way ANOVA followed by Bonferroni’s multiple comparison test. Data for PARP refer to the faster migrating band marked as * and are given relative to samples treated with ERN alone. Blots shown are representative of at least three independent experiments

Techniques Used:

Effect of co-treatment of breast cancer cell lines with 4-hydroxytamoxifen and sulforaphane on PARP cleavage and levels of Bcl-2, Bax, survivin and ADRP. T47D ( a ) and MCF-7 ( b ) cells were treated with 5 μM sulforaphane (SFN), and/or 0.5 μM 4-hydroxytamoxifen (4-OH-T). BT-474 ( c ) cells were treated with 5 μM sulforaphane (SFN) and/or 1 μM 4-hydroxytamoxifen (4-OH-T). Blots were stripped and reprobed with anti-β-actin antibody to ensure equal protein loading. Results are plotted as mean ± SE from three independent experiments, *significantly different compared with single agent-treated samples or **significantly different compared with one of the single agent-treated samples by one-way ANOVA followed by Bonferroni’s multiple comparison test. Data for PARP refer to the faster migrating band marked as * and are given relative to samples treated with SFN alone. Blots shown are representative of at least three independent experiments
Figure Legend Snippet: Effect of co-treatment of breast cancer cell lines with 4-hydroxytamoxifen and sulforaphane on PARP cleavage and levels of Bcl-2, Bax, survivin and ADRP. T47D ( a ) and MCF-7 ( b ) cells were treated with 5 μM sulforaphane (SFN), and/or 0.5 μM 4-hydroxytamoxifen (4-OH-T). BT-474 ( c ) cells were treated with 5 μM sulforaphane (SFN) and/or 1 μM 4-hydroxytamoxifen (4-OH-T). Blots were stripped and reprobed with anti-β-actin antibody to ensure equal protein loading. Results are plotted as mean ± SE from three independent experiments, *significantly different compared with single agent-treated samples or **significantly different compared with one of the single agent-treated samples by one-way ANOVA followed by Bonferroni’s multiple comparison test. Data for PARP refer to the faster migrating band marked as * and are given relative to samples treated with SFN alone. Blots shown are representative of at least three independent experiments

Techniques Used:

65) Product Images from "MicroRNA-34b mediates hippocampal astrocyte apoptosis in a rat model of recurrent seizures"

Article Title: MicroRNA-34b mediates hippocampal astrocyte apoptosis in a rat model of recurrent seizures

Journal: BMC Neuroscience

doi: 10.1186/s12868-016-0291-6

miR-34b-5p regulation of astrocyte apoptosis through mediating Bcl-2 expression level. a , b Western blot analysis for Bcl-2, Bax, pro-caspase-3, and cleaved caspase-3. Cell lysates were prepared from astrocytes treated with vehicle control, mimics negative control (m NC) or inhibitors negative control (i NC), miR-34b-5p mimics or inhibitors. c Bax/Bcl-2 protein ratio after quantitative analysis (one-way ANOVA, n = 5, F 4,20 = 123.8, *** P
Figure Legend Snippet: miR-34b-5p regulation of astrocyte apoptosis through mediating Bcl-2 expression level. a , b Western blot analysis for Bcl-2, Bax, pro-caspase-3, and cleaved caspase-3. Cell lysates were prepared from astrocytes treated with vehicle control, mimics negative control (m NC) or inhibitors negative control (i NC), miR-34b-5p mimics or inhibitors. c Bax/Bcl-2 protein ratio after quantitative analysis (one-way ANOVA, n = 5, F 4,20 = 123.8, *** P

Techniques Used: Expressing, Western Blot, Negative Control

miR-34b-5p promotes KA-induced astrocytes apoptosis by targeting Bcl-2. a Representative images of three repeated TUNEL staining experiments on cultured astrocytes. The astrocytes are pre-treated with of miR-34b-5p mimics, inhibitors, mimics negative control (mNC), and inhibitors negative control (i NC), followed by KA treatment; scale bar 50 μm. b Relative miR-34b-5p levels after different treatments; (one-way ANOVA, n = 5, F 4 ,20 = 866.9, *** P
Figure Legend Snippet: miR-34b-5p promotes KA-induced astrocytes apoptosis by targeting Bcl-2. a Representative images of three repeated TUNEL staining experiments on cultured astrocytes. The astrocytes are pre-treated with of miR-34b-5p mimics, inhibitors, mimics negative control (mNC), and inhibitors negative control (i NC), followed by KA treatment; scale bar 50 μm. b Relative miR-34b-5p levels after different treatments; (one-way ANOVA, n = 5, F 4 ,20 = 866.9, *** P

Techniques Used: TUNEL Assay, Staining, Cell Culture, Negative Control

Cell apoptosis and miR-34b-5p expression induced in rat hippocampus after flurothyl treatments. a Pictures of TUNEL staining (400) showed seizured mice with more cell death in both the CA1 and DG regions. DAB detection; representative of eight mice; scale bars, 100 μm. b Western blotting. Hippocampal tissue protein was extracted from control and flurothyl-treated rats at 2 h, 6 h, 1 day, 3 days, or 7 days after treatments were completed. Bcl-2, Bax, pro-caspase-3, and caspase-3 were blotted for analyses. c Bax/Bcl-2 ratio ( n = 8, comparing seizured rat tissue with control rat tissue at different time points, 2 h: t 14 = 8.53; 6 h: t 14 = 8.33; day 1: t 14 = 12.83; day 3: t 14 = 10.94; day 7: t 14 = 14.72; ***P
Figure Legend Snippet: Cell apoptosis and miR-34b-5p expression induced in rat hippocampus after flurothyl treatments. a Pictures of TUNEL staining (400) showed seizured mice with more cell death in both the CA1 and DG regions. DAB detection; representative of eight mice; scale bars, 100 μm. b Western blotting. Hippocampal tissue protein was extracted from control and flurothyl-treated rats at 2 h, 6 h, 1 day, 3 days, or 7 days after treatments were completed. Bcl-2, Bax, pro-caspase-3, and caspase-3 were blotted for analyses. c Bax/Bcl-2 ratio ( n = 8, comparing seizured rat tissue with control rat tissue at different time points, 2 h: t 14 = 8.53; 6 h: t 14 = 8.33; day 1: t 14 = 12.83; day 3: t 14 = 10.94; day 7: t 14 = 14.72; ***P

Techniques Used: Expressing, TUNEL Assay, Staining, Mouse Assay, Western Blot

66) Product Images from "Morin, a Flavonoid from Moraceae, Induces Apoptosis by Induction of BAD Protein in Human Leukemic Cells"

Article Title: Morin, a Flavonoid from Moraceae, Induces Apoptosis by Induction of BAD Protein in Human Leukemic Cells

Journal: International Journal of Molecular Sciences

doi: 10.3390/ijms16010645

Proposed model of morin mechanism of action for apoptosis in U937 human leukemic cells. Morin induced caspase-dependent apoptosis; induced loss of MMP ( ΔΨ m ) along with cytochrome c release, downregulated Bcl-2 protein, and upregulated BAX proteins. It activates caspase-3 and caspase-9, and subsequent cleavage of PARP. In addition, caspase-3, z-DEVD-fmk reduced morin-induced cell death. Taken together, this study suggests that morin induces caspase-dependent apoptosis through an intrinsic pathway by modulating Bcl-2 family members, BAD and Bcl-xL, which regulates the apoptotic effect of morin in human leukemic cells.
Figure Legend Snippet: Proposed model of morin mechanism of action for apoptosis in U937 human leukemic cells. Morin induced caspase-dependent apoptosis; induced loss of MMP ( ΔΨ m ) along with cytochrome c release, downregulated Bcl-2 protein, and upregulated BAX proteins. It activates caspase-3 and caspase-9, and subsequent cleavage of PARP. In addition, caspase-3, z-DEVD-fmk reduced morin-induced cell death. Taken together, this study suggests that morin induces caspase-dependent apoptosis through an intrinsic pathway by modulating Bcl-2 family members, BAD and Bcl-xL, which regulates the apoptotic effect of morin in human leukemic cells.

Techniques Used:

Effects of Bcl-2 overexpression on morin-induced apoptosis. U937/vector or U937/Bcl-2 cells were treated with morin for 48 h, and effects of Bcl-2 overexpression on morin-induced apoptosis. ( A ) MTT assay. The data are shown as means ± SD of three independent experiments. * p
Figure Legend Snippet: Effects of Bcl-2 overexpression on morin-induced apoptosis. U937/vector or U937/Bcl-2 cells were treated with morin for 48 h, and effects of Bcl-2 overexpression on morin-induced apoptosis. ( A ) MTT assay. The data are shown as means ± SD of three independent experiments. * p

Techniques Used: Over Expression, Plasmid Preparation, MTT Assay

The effects of morin on mitochondrial membrane potential ( ΔΨ m ), and Bcl-2 family members in U937 cells. ( A ) Morin induced Loss of MMP ( ΔΨ m ) in a dose-dependent manner. The cells were stained with JC-1 and incubated at 37 °C for 30 min. The mean JC-1 fluorescence intensity was assessed by a flow cytometer; ( B , C ) The effects of morin on the expression of ( B ) death receptors ( C ) Bcl-2 and IAP family members in U937 cells. The results are from one representative of two independent experiments that showed similar patterns. The expression of the indicated proteins were measured by densitometry and expressed as average relative ratio compared to actin, from two or three different experiments.
Figure Legend Snippet: The effects of morin on mitochondrial membrane potential ( ΔΨ m ), and Bcl-2 family members in U937 cells. ( A ) Morin induced Loss of MMP ( ΔΨ m ) in a dose-dependent manner. The cells were stained with JC-1 and incubated at 37 °C for 30 min. The mean JC-1 fluorescence intensity was assessed by a flow cytometer; ( B , C ) The effects of morin on the expression of ( B ) death receptors ( C ) Bcl-2 and IAP family members in U937 cells. The results are from one representative of two independent experiments that showed similar patterns. The expression of the indicated proteins were measured by densitometry and expressed as average relative ratio compared to actin, from two or three different experiments.

Techniques Used: Staining, Incubation, Fluorescence, Flow Cytometry, Cytometry, Expressing

67) Product Images from "SAG-UPS attenuates proapoptotic SARM and Noxa to confer survival advantage to early hepatocellular carcinoma"

Article Title: SAG-UPS attenuates proapoptotic SARM and Noxa to confer survival advantage to early hepatocellular carcinoma

Journal: Cell Death Discovery

doi: 10.1038/cddiscovery.2015.32

SAG overexpression in HCC cells attenuates proapoptotic Noxa and SARM. To further confirm the critical regulator(s) in liver cancer, we characterized the expression profiles of proapoptotic (Noxa, SARM and Bax) and antiapoptotic (SAG, Bcl-2 and Bcl-xL) factors in six human HCC cell lines. Consistent with primary HCC, immunoblottings showed reciprocal relationship in both Noxa/SAG and SARM/SAG in HCC cell lines ( a , blue and red box). To confirm whether Noxa and SARM are regulated by SAG-dependent protein degradation, HA-SAG was transiently transfected and overexpressed in HCC cells, followed by immunoblotting analysis ( b ) and real-time PCR ( c ). SAG overexpression attenuated both Noxa and SARM proteins throughout six tested HCC cell lines (shown as arrows), but not Bcl-2 and Bcl-xL. Bax was found to be decreased in Huh7 and Hep3B cells, and increased in SNU449, when SAG was overexpressed. Real-time PCR affirms that attenuated Noxa and SARM under SAG overexpression is due to a post-transcriptional event, suggesting the involvement of SAG-dependent UPS. Actin was used as a loading control for immunoblotting. qRT-PCR values are normalized using human β 2-microglobulin gene and presented as means±S.D. ( n =3).
Figure Legend Snippet: SAG overexpression in HCC cells attenuates proapoptotic Noxa and SARM. To further confirm the critical regulator(s) in liver cancer, we characterized the expression profiles of proapoptotic (Noxa, SARM and Bax) and antiapoptotic (SAG, Bcl-2 and Bcl-xL) factors in six human HCC cell lines. Consistent with primary HCC, immunoblottings showed reciprocal relationship in both Noxa/SAG and SARM/SAG in HCC cell lines ( a , blue and red box). To confirm whether Noxa and SARM are regulated by SAG-dependent protein degradation, HA-SAG was transiently transfected and overexpressed in HCC cells, followed by immunoblotting analysis ( b ) and real-time PCR ( c ). SAG overexpression attenuated both Noxa and SARM proteins throughout six tested HCC cell lines (shown as arrows), but not Bcl-2 and Bcl-xL. Bax was found to be decreased in Huh7 and Hep3B cells, and increased in SNU449, when SAG was overexpressed. Real-time PCR affirms that attenuated Noxa and SARM under SAG overexpression is due to a post-transcriptional event, suggesting the involvement of SAG-dependent UPS. Actin was used as a loading control for immunoblotting. qRT-PCR values are normalized using human β 2-microglobulin gene and presented as means±S.D. ( n =3).

Techniques Used: Over Expression, Expressing, Transfection, Real-time Polymerase Chain Reaction, Quantitative RT-PCR

68) Product Images from "Adeno-sh-?-Catenin Abolishes Ischemic Preconditioning-Mediated Cardioprotection by Downregulation of Its Target Genes VEGF, Bcl-2, and Survivin in Ischemic Rat Myocardium"

Article Title: Adeno-sh-?-Catenin Abolishes Ischemic Preconditioning-Mediated Cardioprotection by Downregulation of Its Target Genes VEGF, Bcl-2, and Survivin in Ischemic Rat Myocardium

Journal: Antioxidants & Redox Signaling

doi: 10.1089/ars.2008.2042

Representative bar graphs showing the various mRNA expression. ( A ) VEGF. ( B ) Bcl-2. ( C ) Survivin. * p
Figure Legend Snippet: Representative bar graphs showing the various mRNA expression. ( A ) VEGF. ( B ) Bcl-2. ( C ) Survivin. * p

Techniques Used: Expressing

Representative Western blot showing the expression of VEGF, Bcl-2, and survivin in the cytosolic fraction. GAPDH was used as the loading control. Bar graph represents the quantitative comparison between the groups for VEGF, Bcl-2, and survivin. * p
Figure Legend Snippet: Representative Western blot showing the expression of VEGF, Bcl-2, and survivin in the cytosolic fraction. GAPDH was used as the loading control. Bar graph represents the quantitative comparison between the groups for VEGF, Bcl-2, and survivin. * p

Techniques Used: Western Blot, Expressing

69) Product Images from "Adeno-sh-?-Catenin Abolishes Ischemic Preconditioning-Mediated Cardioprotection by Downregulation of Its Target Genes VEGF, Bcl-2, and Survivin in Ischemic Rat Myocardium"

Article Title: Adeno-sh-?-Catenin Abolishes Ischemic Preconditioning-Mediated Cardioprotection by Downregulation of Its Target Genes VEGF, Bcl-2, and Survivin in Ischemic Rat Myocardium

Journal: Antioxidants & Redox Signaling

doi: 10.1089/ars.2008.2042

Representative bar graphs showing the various mRNA expression. ( A ) VEGF. ( B ) Bcl-2. ( C ) Survivin. * p
Figure Legend Snippet: Representative bar graphs showing the various mRNA expression. ( A ) VEGF. ( B ) Bcl-2. ( C ) Survivin. * p

Techniques Used: Expressing

Representative Western blot showing the expression of VEGF, Bcl-2, and survivin in the cytosolic fraction. GAPDH was used as the loading control. Bar graph represents the quantitative comparison between the groups for VEGF, Bcl-2, and survivin. * p
Figure Legend Snippet: Representative Western blot showing the expression of VEGF, Bcl-2, and survivin in the cytosolic fraction. GAPDH was used as the loading control. Bar graph represents the quantitative comparison between the groups for VEGF, Bcl-2, and survivin. * p

Techniques Used: Western Blot, Expressing

70) Product Images from "Small Interfering RNA Targeting Heme Oxygenase-1 (HO-1) Reinforces Liver Apoptosis Induced by Ischemia-Reperfusion Injury in Mice: HO-1 Is Necessary for Cytoprotection"

Article Title: Small Interfering RNA Targeting Heme Oxygenase-1 (HO-1) Reinforces Liver Apoptosis Induced by Ischemia-Reperfusion Injury in Mice: HO-1 Is Necessary for Cytoprotection

Journal: Human Gene Therapy

doi: 10.1089/hum.2009.049

Western blot analysis of HO-1, caspase-3, Bcl-2, and Bcl-x L gene products in hepatic lobes 6 hr after 90 min of warm ischemia. Lane 1, sham; lane 2, HO-1 siRNA; lane 3, nonspecific siRNA; lane 4, Ad-HO-1; lane 5, Ad-β-gal. Note the selectively decreased expression of HO-1 and Bcl-2/Bcl-x L , and markedly increased caspase-3, in mice treated with HO-1 siRNA as compared with those conditioned with nonspecific siRNA or Ad-HO-1. In contrast, Ad-HO-1 increased the expression of HO-1 and Bcl-2/Bcl-x L , and decreased that of caspase-3. Data shown are representative of three separate experiments.
Figure Legend Snippet: Western blot analysis of HO-1, caspase-3, Bcl-2, and Bcl-x L gene products in hepatic lobes 6 hr after 90 min of warm ischemia. Lane 1, sham; lane 2, HO-1 siRNA; lane 3, nonspecific siRNA; lane 4, Ad-HO-1; lane 5, Ad-β-gal. Note the selectively decreased expression of HO-1 and Bcl-2/Bcl-x L , and markedly increased caspase-3, in mice treated with HO-1 siRNA as compared with those conditioned with nonspecific siRNA or Ad-HO-1. In contrast, Ad-HO-1 increased the expression of HO-1 and Bcl-2/Bcl-x L , and decreased that of caspase-3. Data shown are representative of three separate experiments.

Techniques Used: Western Blot, Expressing, Mouse Assay

71) Product Images from "Cyanide-induced Death of Dopaminergic Cells is Mediated by Uncoupling Protein-2 Up-regulation and Reduced Bcl-2 Expression"

Article Title: Cyanide-induced Death of Dopaminergic Cells is Mediated by Uncoupling Protein-2 Up-regulation and Reduced Bcl-2 Expression

Journal: Toxicology and applied pharmacology

doi: 10.1016/j.taap.2009.03.020

Effect of UCP-2 knockdown on Bcl-2 expression and cyanide toxicity. Cells were transfected with UCP-2 RNAi and 24 h later treated with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 12 h. (A) Bcl-2 levels as detected by Western
Figure Legend Snippet: Effect of UCP-2 knockdown on Bcl-2 expression and cyanide toxicity. Cells were transfected with UCP-2 RNAi and 24 h later treated with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 12 h. (A) Bcl-2 levels as detected by Western

Techniques Used: Expressing, Transfection, Western Blot

Effect of Bcl-2 over-expression on cyanide toxicity following UCP-2 up-regulation. 24 h after transfection with a Bcl-2 + expression plasmid, cells were treated with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 24 h. (A) Cells
Figure Legend Snippet: Effect of Bcl-2 over-expression on cyanide toxicity following UCP-2 up-regulation. 24 h after transfection with a Bcl-2 + expression plasmid, cells were treated with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 24 h. (A) Cells

Techniques Used: Over Expression, Transfection, Expressing, Plasmid Preparation

Effect of mtGSH repletion on H 2 O 2 accumulation and Bcl-2 down-regulation. Cells were pre-loaded with GSH-EE (2 mM) for 1 h and then treated with Wy14,643 (100 μM) for 5 h followed by KCN (400 μM) for 12 h. (A) Cytosolic and mitochondrial
Figure Legend Snippet: Effect of mtGSH repletion on H 2 O 2 accumulation and Bcl-2 down-regulation. Cells were pre-loaded with GSH-EE (2 mM) for 1 h and then treated with Wy14,643 (100 μM) for 5 h followed by KCN (400 μM) for 12 h. (A) Cytosolic and mitochondrial

Techniques Used:

Effect of UCP-2 regulation on Bcl-2 expression. (A) Cells were treated with Wy14,643 (25–200 μM) for 12 h, and then UCP-2 and Bcl-2 expression determined by Western blot analysis. (B) Time course of UCP-2 and Bcl-2 expression after treatment
Figure Legend Snippet: Effect of UCP-2 regulation on Bcl-2 expression. (A) Cells were treated with Wy14,643 (25–200 μM) for 12 h, and then UCP-2 and Bcl-2 expression determined by Western blot analysis. (B) Time course of UCP-2 and Bcl-2 expression after treatment

Techniques Used: Expressing, Western Blot

Effect of cyanide on Bcl-2 expression after UCP-2 up-regulation or over-expression. (A) UCP-2 was up-regulated by Wy14,643 (100 μM) treatment for 5 h, followed by KCN (400 μM) for 12 h. Cellular Bcl-2 expression was determined by Western
Figure Legend Snippet: Effect of cyanide on Bcl-2 expression after UCP-2 up-regulation or over-expression. (A) UCP-2 was up-regulated by Wy14,643 (100 μM) treatment for 5 h, followed by KCN (400 μM) for 12 h. Cellular Bcl-2 expression was determined by Western

Techniques Used: Expressing, Over Expression, Western Blot

Effect of cyanide on Bcl-2 mRNA levels and proteasomal metabolism following UCP-2 up-regulation. (A) Bcl-2 mRNA expression was determined by real-time PCR analysis. (B) Western analysis of whole cell ubiquinated proteins was determined by blotting with
Figure Legend Snippet: Effect of cyanide on Bcl-2 mRNA levels and proteasomal metabolism following UCP-2 up-regulation. (A) Bcl-2 mRNA expression was determined by real-time PCR analysis. (B) Western analysis of whole cell ubiquinated proteins was determined by blotting with

Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Western Blot

Cyanide-mediated changes in intracellular hydrogen peroxide generation and Bcl-2 expression. (A) Cellular levels of H 2 O 2 after treatment with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 12 h. H 2 O 2 was detected by the Amplex
Figure Legend Snippet: Cyanide-mediated changes in intracellular hydrogen peroxide generation and Bcl-2 expression. (A) Cellular levels of H 2 O 2 after treatment with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 12 h. H 2 O 2 was detected by the Amplex

Techniques Used: Expressing

72) Product Images from "Cyanide-induced Death of Dopaminergic Cells is Mediated by Uncoupling Protein-2 Up-regulation and Reduced Bcl-2 Expression"

Article Title: Cyanide-induced Death of Dopaminergic Cells is Mediated by Uncoupling Protein-2 Up-regulation and Reduced Bcl-2 Expression

Journal: Toxicology and applied pharmacology

doi: 10.1016/j.taap.2009.03.020

Effect of UCP-2 knockdown on Bcl-2 expression and cyanide toxicity. Cells were transfected with UCP-2 RNAi and 24 h later treated with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 12 h. (A) Bcl-2 levels as detected by Western
Figure Legend Snippet: Effect of UCP-2 knockdown on Bcl-2 expression and cyanide toxicity. Cells were transfected with UCP-2 RNAi and 24 h later treated with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 12 h. (A) Bcl-2 levels as detected by Western

Techniques Used: Expressing, Transfection, Western Blot

Effect of Bcl-2 over-expression on cyanide toxicity following UCP-2 up-regulation. 24 h after transfection with a Bcl-2 + expression plasmid, cells were treated with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 24 h. (A) Cells
Figure Legend Snippet: Effect of Bcl-2 over-expression on cyanide toxicity following UCP-2 up-regulation. 24 h after transfection with a Bcl-2 + expression plasmid, cells were treated with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 24 h. (A) Cells

Techniques Used: Over Expression, Transfection, Expressing, Plasmid Preparation

Effect of mtGSH repletion on H 2 O 2 accumulation and Bcl-2 down-regulation. Cells were pre-loaded with GSH-EE (2 mM) for 1 h and then treated with Wy14,643 (100 μM) for 5 h followed by KCN (400 μM) for 12 h. (A) Cytosolic and mitochondrial
Figure Legend Snippet: Effect of mtGSH repletion on H 2 O 2 accumulation and Bcl-2 down-regulation. Cells were pre-loaded with GSH-EE (2 mM) for 1 h and then treated with Wy14,643 (100 μM) for 5 h followed by KCN (400 μM) for 12 h. (A) Cytosolic and mitochondrial

Techniques Used:

Effect of UCP-2 regulation on Bcl-2 expression. (A) Cells were treated with Wy14,643 (25–200 μM) for 12 h, and then UCP-2 and Bcl-2 expression determined by Western blot analysis. (B) Time course of UCP-2 and Bcl-2 expression after treatment
Figure Legend Snippet: Effect of UCP-2 regulation on Bcl-2 expression. (A) Cells were treated with Wy14,643 (25–200 μM) for 12 h, and then UCP-2 and Bcl-2 expression determined by Western blot analysis. (B) Time course of UCP-2 and Bcl-2 expression after treatment

Techniques Used: Expressing, Western Blot

Effect of cyanide on Bcl-2 expression after UCP-2 up-regulation or over-expression. (A) UCP-2 was up-regulated by Wy14,643 (100 μM) treatment for 5 h, followed by KCN (400 μM) for 12 h. Cellular Bcl-2 expression was determined by Western
Figure Legend Snippet: Effect of cyanide on Bcl-2 expression after UCP-2 up-regulation or over-expression. (A) UCP-2 was up-regulated by Wy14,643 (100 μM) treatment for 5 h, followed by KCN (400 μM) for 12 h. Cellular Bcl-2 expression was determined by Western

Techniques Used: Expressing, Over Expression, Western Blot

Effect of cyanide on Bcl-2 mRNA levels and proteasomal metabolism following UCP-2 up-regulation. (A) Bcl-2 mRNA expression was determined by real-time PCR analysis. (B) Western analysis of whole cell ubiquinated proteins was determined by blotting with
Figure Legend Snippet: Effect of cyanide on Bcl-2 mRNA levels and proteasomal metabolism following UCP-2 up-regulation. (A) Bcl-2 mRNA expression was determined by real-time PCR analysis. (B) Western analysis of whole cell ubiquinated proteins was determined by blotting with

Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Western Blot

Cyanide-mediated changes in intracellular hydrogen peroxide generation and Bcl-2 expression. (A) Cellular levels of H 2 O 2 after treatment with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 12 h. H 2 O 2 was detected by the Amplex
Figure Legend Snippet: Cyanide-mediated changes in intracellular hydrogen peroxide generation and Bcl-2 expression. (A) Cellular levels of H 2 O 2 after treatment with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 12 h. H 2 O 2 was detected by the Amplex

Techniques Used: Expressing

73) Product Images from "β-Sitosterol targets Trx/Trx1 reductase to induce apoptosis in A549 cells via ROS mediated mitochondrial dysregulation and p53 activation"

Article Title: β-Sitosterol targets Trx/Trx1 reductase to induce apoptosis in A549 cells via ROS mediated mitochondrial dysregulation and p53 activation

Journal: Scientific Reports

doi: 10.1038/s41598-018-20311-6

BS induced apoptosis occurred via mitochondrial membrane permeability loss and releases of apoptogenic factors. ( a ) Loss of ΔΨ m in A549 cells at different time points of BS treatment (25 μM) were imaged by Rhodamine 123 staining. ( b ) Fluorescence spectroscopy analysis of Rhodamine 123 stained BS treated cells. ( c ) Up-regulation of bax and cytochrome c was detected upon BS treatment, while significant down-regulation of bcl-2 was also observed after 72 h incubation. ( d ) Relative protein expression of bcl-2 family protein and cytochrome c release. The gel blots were cropped from different gels and the full length blots are given in the supplementary file. **P
Figure Legend Snippet: BS induced apoptosis occurred via mitochondrial membrane permeability loss and releases of apoptogenic factors. ( a ) Loss of ΔΨ m in A549 cells at different time points of BS treatment (25 μM) were imaged by Rhodamine 123 staining. ( b ) Fluorescence spectroscopy analysis of Rhodamine 123 stained BS treated cells. ( c ) Up-regulation of bax and cytochrome c was detected upon BS treatment, while significant down-regulation of bcl-2 was also observed after 72 h incubation. ( d ) Relative protein expression of bcl-2 family protein and cytochrome c release. The gel blots were cropped from different gels and the full length blots are given in the supplementary file. **P

Techniques Used: Permeability, Staining, Fluorescence, Spectroscopy, Incubation, Expressing

74) Product Images from "Simultaneous gene silencing of Bcl-2, XIAP and Survivin re-sensitizes pancreatic cancer cells towards apoptosis"

Article Title: Simultaneous gene silencing of Bcl-2, XIAP and Survivin re-sensitizes pancreatic cancer cells towards apoptosis

Journal: BMC Cancer

doi: 10.1186/1471-2407-10-379

Gene-silencing of Bcl-2, Survivin and XIAP . Western blot showed efficient silencing in transfected MiaPaCa-2 ( A ) and AsPC-1 cells ( B ). 50,000 cells/well were single-transfected with carrier solution (lane 1) and siRNA against Luciferase (lane 2) as control. SGS, lowST and ST all effectively silenced the three target genes (lane 3-5). Efficient knock-down was also shown in the lowST group by RT-PCR in MiaPaCa-2 ( C ) and AsPC-1 cells ( D ). White bars show controls, grey bars signify transfected cells. All samples were normalized to β-Actin as a house-keeping gene. SGS = Simultaneous gene silencing; lowST = Low dose siRNA transfection; ST = Standard dose siRNA transfection.
Figure Legend Snippet: Gene-silencing of Bcl-2, Survivin and XIAP . Western blot showed efficient silencing in transfected MiaPaCa-2 ( A ) and AsPC-1 cells ( B ). 50,000 cells/well were single-transfected with carrier solution (lane 1) and siRNA against Luciferase (lane 2) as control. SGS, lowST and ST all effectively silenced the three target genes (lane 3-5). Efficient knock-down was also shown in the lowST group by RT-PCR in MiaPaCa-2 ( C ) and AsPC-1 cells ( D ). White bars show controls, grey bars signify transfected cells. All samples were normalized to β-Actin as a house-keeping gene. SGS = Simultaneous gene silencing; lowST = Low dose siRNA transfection; ST = Standard dose siRNA transfection.

Techniques Used: Western Blot, Transfection, Luciferase, Reverse Transcription Polymerase Chain Reaction

75) Product Images from "IGF-IR dependent expression of Survivin is required for T-Antigen mediated Protection from Apoptosis and Proliferation of Neural Progenitors"

Article Title: IGF-IR dependent expression of Survivin is required for T-Antigen mediated Protection from Apoptosis and Proliferation of Neural Progenitors

Journal: Cell death and differentiation

doi: 10.1038/cdd.2009.146

Immunohistochemical characterization of IGF-IR knockout mouse embryos IGF-IR knockout embryos are smaller in size and volume than their wild type littermates (Montages). The brain of wild type animals is considerably bigger, contains several flexures and is well layered, while knockout mice have thinner, flatter and less differentiated brains. While the brain and DRG of wild type animals contains bigger neurons with abundant cytoplasm, knockout mice contains smaller and more primitive neurons with scant cytoplasm (upper panels, Hematoxylin Eosin). The anti-apoptotic protein Survivin is expressed abundantly in the brain and dorsal root ganglia (DRG) of wild type mice, where no apoptosis is detected by TUNEL assay. IGF-IR knockout mice demonstrate very weak and low levels of Survivin, and show numerous cells undergoing apoptosis. The levels of Survivin also correlate with the degree of differentiation. While the early marker Nestin is detected in low levels in wild type brain and DRG, its expression is robust in the smaller neurons of the knockout mice, in an inverse relation to the later neuronal marker class III β-Tubulin, which is abundant and robust in larger neurons of wild type brain and DRG, indicating a higher degree of differentiation. Other anti-apoptotic pathways, including Bcl-2 demonstrated no significant differences between the wild type and knockout brains and dorsal root ganglia (lower panels). Original magnification for all brain panels ×200. All DRG panels ×400.
Figure Legend Snippet: Immunohistochemical characterization of IGF-IR knockout mouse embryos IGF-IR knockout embryos are smaller in size and volume than their wild type littermates (Montages). The brain of wild type animals is considerably bigger, contains several flexures and is well layered, while knockout mice have thinner, flatter and less differentiated brains. While the brain and DRG of wild type animals contains bigger neurons with abundant cytoplasm, knockout mice contains smaller and more primitive neurons with scant cytoplasm (upper panels, Hematoxylin Eosin). The anti-apoptotic protein Survivin is expressed abundantly in the brain and dorsal root ganglia (DRG) of wild type mice, where no apoptosis is detected by TUNEL assay. IGF-IR knockout mice demonstrate very weak and low levels of Survivin, and show numerous cells undergoing apoptosis. The levels of Survivin also correlate with the degree of differentiation. While the early marker Nestin is detected in low levels in wild type brain and DRG, its expression is robust in the smaller neurons of the knockout mice, in an inverse relation to the later neuronal marker class III β-Tubulin, which is abundant and robust in larger neurons of wild type brain and DRG, indicating a higher degree of differentiation. Other anti-apoptotic pathways, including Bcl-2 demonstrated no significant differences between the wild type and knockout brains and dorsal root ganglia (lower panels). Original magnification for all brain panels ×200. All DRG panels ×400.

Techniques Used: Immunohistochemistry, Knock-Out, Mouse Assay, TUNEL Assay, Marker, Expressing

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Nucleic Acid Electrophoresis:

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SYBR Green Assay:

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Incubation:

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Activity Assay:

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Expressing:

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BIA-KA:

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Modification:

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Planar Chromatography:

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Transfection:

Article Title: JARID1B deletion induced apoptosis in Jeko-1 and HL-60 cell lines
Article Snippet: Briefly, Jeko-1 and HL-60 cells were plated on culture dishes and transfected by JARID1B siRNA with 60, 120, 240 nmol/L for 24 hours. .. Membranes were incubated with monoclonal anti-tri-methylated-histoneH3K4, anti-histone acetylation of H3, H4, JARID1B (Upstate, UAS), BCL-2, proaspase-3, C-myc, cyclin D1 (Santa Cruz USA).

Synthesized:

Article Title: Dihydroartemisinin and its derivative induce apoptosis in acute myeloid leukemia through Noxa-mediated pathway requiring iron and endoperoxide moiety
Article Snippet: Reagents X-11, DODHA (deoxy-dihydroartemisinin), and DOX-11 (10-O-[4-(1-acetyl-5-phenyl-4,5-dihydropyrazol-3-yl) phenyl]-(10S)-deoxy-dihydroartemisinin) were synthesized as described in . .. Antibodies to poly-(ADP-ribose)-polymerase (PARP), caspase-3 and caspase-8 were obtained from BD Biosciences (San Diego, CA); to Mcl-1, Bcl-2, Bcl-xL, Bax, and β-actin were from Santa Cruz Biotechology, Inc. (Santa Cruz, CA); to Bim, Bak, CHOP, FOXO3a, Puma, cleaved caspase-9 and -3 were from Cell Signaling Technology, Inc. (Beverly, MA); and to Noxa was from Abcam Inc. (Cambridge, MA).

Article Title: Para amino benzoic acid-derived self-assembled biocompatible nanoparticles for efficient delivery of siRNA
Article Snippet: Custom-designed Bcl-2 and β-actin polymerase chain reaction (PCR) primers were synthesized by Eurofins, (New Orleans, LA, USA). .. Rabbit monoclonal primary antibody for Bcl-2 and mouse monoclonal antibody β-actin were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA) and Abcam (Cambridge, MA, USA), respectively.

Cell Culture:

Article Title: Inhibition of IkB kinase and NF-kB by a novel synthetic compound SK 2009
Article Snippet: The cell line KBM-5 (human chronic myeloid leukemia) was obtained from the American Type Culture Collection and was cultured in Iscove’s modified Dulbecco’s medium with 15% FBS. .. Antibodies against cyclin D1, Bcl-2 and VEGF were obtained from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

Article Title: Molecular mechanisms underlying the antitumor activity of (E)-N-hydroxy-3-(1-(4-methoxyphenylsulfonyl)-1,2,3,4-tetrahydroquinolin-6-yl)acrylamide in human colorectal cancer cells in vitro and in vivo
Article Snippet: Paragraph title: Cell culture and reagents ... Antibodies against various proteins were obtained from the following sources: PARP (Poly-ADP-ribose polymerase), Mcl-1, Bcl-2, Bcl-XL, survivin, cytochrome c, Bax, Bak, Bim, anti-mouse and anti-rabbit IgGs were obtained from Santa Cruz Biotechnology Inc. (Santa Cruz, CA, USA).

Protein Concentration:

Article Title: JARID1B deletion induced apoptosis in Jeko-1 and HL-60 cell lines
Article Snippet: Membranes were incubated with monoclonal anti-tri-methylated-histoneH3K4, anti-histone acetylation of H3, H4, JARID1B (Upstate, UAS), BCL-2, proaspase-3, C-myc, cyclin D1 (Santa Cruz USA). .. Membranes were incubated with monoclonal anti-tri-methylated-histoneH3K4, anti-histone acetylation of H3, H4, JARID1B (Upstate, UAS), BCL-2, proaspase-3, C-myc, cyclin D1 (Santa Cruz USA).

Sequencing:

Article Title: Para amino benzoic acid-derived self-assembled biocompatible nanoparticles for efficient delivery of siRNA
Article Snippet: Bcl-2 primer sequence forward primer 5′-GGG GAG AAG GT G TTC ATT CA-3′, reverse primer 5′-CAA CTC TTT TCC TCC CAC CA-3′ β-actin primer sequence forward primer 5′-AGA GGG AAA TCG TGC GTG AC-3′, reverse primer 5′-CAATA GTGAT GACCT GGCCGT-3′. .. Rabbit monoclonal primary antibody for Bcl-2 and mouse monoclonal antibody β-actin were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA) and Abcam (Cambridge, MA, USA), respectively.

Recombinant:

Article Title: Inhibition of IkB kinase and NF-kB by a novel synthetic compound SK 2009
Article Snippet: Bacteria-derived human recombinant human TNFα, purified to homogeneity with a specific activity of 5 × 107 U/mg, was kindly provided by Genentech (South San Francisco, CA, USA). .. Antibodies against cyclin D1, Bcl-2 and VEGF were obtained from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

Article Title: Astragalus polysaccharides suppress ICAM-1 and VCAM-1 expression in TNF-α-treated human vascular endothelial cells by blocking NF-κB activation
Article Snippet: Anti-ICAM-1, VCAM-1, NF-κB, phosphorylated-NF-κB, IκBα, phosphorylated-IκBα, Bax, Bcl-2, and MCP-1 antibodies were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA). .. Recombinant human TNF-α was obtained from Peprotech (Rocky Hill, NJ, USA).

MTT Assay:

Article Title: Molecular mechanisms underlying the antitumor activity of (E)-N-hydroxy-3-(1-(4-methoxyphenylsulfonyl)-1,2,3,4-tetrahydroquinolin-6-yl)acrylamide in human colorectal cancer cells in vitro and in vivo
Article Snippet: 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), propidium iodide (PI), zVAD and all of the other chemical reagents were purchased from Sigma Chemical (St. Louis, MO, USA). .. Antibodies against various proteins were obtained from the following sources: PARP (Poly-ADP-ribose polymerase), Mcl-1, Bcl-2, Bcl-XL, survivin, cytochrome c, Bax, Bak, Bim, anti-mouse and anti-rabbit IgGs were obtained from Santa Cruz Biotechnology Inc. (Santa Cruz, CA, USA).

Multiple Displacement Amplification:

Article Title: Para amino benzoic acid-derived self-assembled biocompatible nanoparticles for efficient delivery of siRNA
Article Snippet: Rabbit monoclonal primary antibody for Bcl-2 and mouse monoclonal antibody β-actin were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA) and Abcam (Cambridge, MA, USA), respectively. .. A HeLa human cervical cancer cell line was sourced from the American Type Culture Collection (Manassas, VA, USA) and an RFP-stable MDA-MB-231 reporter cell line was purchased from Cell Biolabs (San Diego, CA, USA).

Article Title: 17β-estradiol and tamoxifen protect mice from manganese-induced dopaminergic neurotoxicity
Article Snippet: Antibodies for TH (sc-25269), transforming growth factor-α (TGF-α, sc-36), ER-α (sc-542), catalase (CAT, sc-271803), Bax (sc-7480), Bcl-2 (sc-7382) and β-actin (sc-47778) were acquired from Santa Cruz Biotechnology (Santa Cruz, CA). .. Malondialdehyde (MDA)/lipid peroxidation/TBARS assay kit (Cat. # 10009055) was obtained from Cayman Chemical (Ann Arbor, MI).

Western Blot:

Article Title: Melatonin Treatment Regulates SIRT3 Expression in Early Brain Injury (EBI) Due to Reactive Oxygen Species (ROS) in a Mouse Model of Subarachnoid Hemorrhage (SAH)
Article Snippet: Paragraph title: Western blot analysis ... The nitrocellulose membranes were incubated with the primary antibodies to Sirt3, Bax, Bcl-2, superoxide dismutase (SOD), and cleaved caspase-3 (1: 4,000 dilution) (Santa Cruz, Biotech) and a primary antibody against β-actin (1: 8,000 dilution, Santa Cruz, Biotech) for 12 hours at 4°C, followed by two hours of incubation at room temperature with the secondary antibodies (1: 5,000 dilution) (Sigma-Aldrich Co., USA).

Article Title: JARID1B deletion induced apoptosis in Jeko-1 and HL-60 cell lines
Article Snippet: Paragraph title: Western blot analysis ... Membranes were incubated with monoclonal anti-tri-methylated-histoneH3K4, anti-histone acetylation of H3, H4, JARID1B (Upstate, UAS), BCL-2, proaspase-3, C-myc, cyclin D1 (Santa Cruz USA).

Article Title: Psoralidin, An Herbal Molecule Inhibits PI3K Mediated Akt Signaling In Androgen Independent Prostate Cancer (AIPC) Cells
Article Snippet: .. PC-3 and DU-145 cells were treated with psoralidin for varying time intervals or doses, whole cell lysates or nuclear and cytoplasmic extracts were obtained and subjected to Western blot analysis using antibodies Akt, NF-κB p50, p65, IκB-α, pIkB-α, IKKα, IKKβ, pIKKα/β, NIK, Bcl-2, , cyclin-D1, GSK-3 and Bax from Santa Cruz Biotechnology (Santa Cruz, CA), PI3 kinase p85, p110, and pAkt from Cell Signaling technology (Danvers, MA) and Bcl-xL from MBL International (Woburn, MA). β-actin and h (Santa Cruz Biotechnology) were used as the internal loading control. .. PC-3 and DU-145 cells were treated with psoralidin or vehicle (DMSO) at different time intervals, cell lysates were immunoprecipitated using PI3 kinase antibody from Upstate USA, Inc. (Chicago, IL) and the immunoprecipitated samples were subjected to Western blot analysis using PI3 kinase p85 and p110 antibodies from Cell Signaling technology (Danvers, MA).

Purification:

Article Title: Inhibition of IkB kinase and NF-kB by a novel synthetic compound SK 2009
Article Snippet: Bacteria-derived human recombinant human TNFα, purified to homogeneity with a specific activity of 5 × 107 U/mg, was kindly provided by Genentech (South San Francisco, CA, USA). .. Antibodies against cyclin D1, Bcl-2 and VEGF were obtained from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

Polymerase Chain Reaction:

Article Title: Para amino benzoic acid-derived self-assembled biocompatible nanoparticles for efficient delivery of siRNA
Article Snippet: Custom-designed Bcl-2 and β-actin polymerase chain reaction (PCR) primers were synthesized by Eurofins, (New Orleans, LA, USA). .. Rabbit monoclonal primary antibody for Bcl-2 and mouse monoclonal antibody β-actin were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA) and Abcam (Cambridge, MA, USA), respectively.

Polyacrylamide Gel Electrophoresis:

Article Title: Melatonin Treatment Regulates SIRT3 Expression in Early Brain Injury (EBI) Due to Reactive Oxygen Species (ROS) in a Mouse Model of Subarachnoid Hemorrhage (SAH)
Article Snippet: The samples were then separated using 8–12% SDS-polyacrylamide gel electrophoresis (PAGE) and transferred to nitrocellulose membranes (Amersham Biosciences, Piscataway, NJ, USA), then incubated at 37 °C for 60 min in a Tris-buffered saline (TBS) containing 10% nonfat dried milk powder and 0.1% Tween20 to eliminate nonspecific antibody binding. .. The nitrocellulose membranes were incubated with the primary antibodies to Sirt3, Bax, Bcl-2, superoxide dismutase (SOD), and cleaved caspase-3 (1: 4,000 dilution) (Santa Cruz, Biotech) and a primary antibody against β-actin (1: 8,000 dilution, Santa Cruz, Biotech) for 12 hours at 4°C, followed by two hours of incubation at room temperature with the secondary antibodies (1: 5,000 dilution) (Sigma-Aldrich Co., USA).

Chloramphenicol Acetyltransferase Assay:

Article Title: Dihydroartemisinin and its derivative induce apoptosis in acute myeloid leukemia through Noxa-mediated pathway requiring iron and endoperoxide moiety
Article Snippet: DHA, acridine orange (AO), ethidium bromide (EB), N-acetylcysteine (NAC) and catalase (CAT), ferrous sulfate (Fe2+ ), ferric ammonium citrate (Fe3+ ), diphenyleneiodonium chloride (DPI) and deferoxamine mesylate (DFO) were purchased from Sigma Chemical Co. (St. Louis, MO). .. Antibodies to poly-(ADP-ribose)-polymerase (PARP), caspase-3 and caspase-8 were obtained from BD Biosciences (San Diego, CA); to Mcl-1, Bcl-2, Bcl-xL, Bax, and β-actin were from Santa Cruz Biotechology, Inc. (Santa Cruz, CA); to Bim, Bak, CHOP, FOXO3a, Puma, cleaved caspase-9 and -3 were from Cell Signaling Technology, Inc. (Beverly, MA); and to Noxa was from Abcam Inc. (Cambridge, MA).

Article Title: 17β-estradiol and tamoxifen protect mice from manganese-induced dopaminergic neurotoxicity
Article Snippet: .. Antibodies for TH (sc-25269), transforming growth factor-α (TGF-α, sc-36), ER-α (sc-542), catalase (CAT, sc-271803), Bax (sc-7480), Bcl-2 (sc-7382) and β-actin (sc-47778) were acquired from Santa Cruz Biotechnology (Santa Cruz, CA). .. Rabbit anti-mouse IgG H & L horseradish peroxidase (HRP)-conjugated (ab6728), Goat anti-rabbit IgG H & L HRP-conjugated (ab97051) and donkey anti-goat (ab97110) IgG H & L horseradish peroxidase (HRP)-conjugated and goat anti-mouse IgG Alexa Fluor® 568 (ab150119) secondary antibodies were obtained from Abcam.

Mouse Assay:

Article Title: Oral treatment with the herbal formula B307 alleviates cardiac toxicity in doxorubicin-treated mice via suppressing oxidative stress, inflammation, and apoptosis
Article Snippet: .. As to the DOX-treated mice, cardiac expression levels of Bcl-2 were visibly enhanced under oral B307 treatment. .. On the other hand, cardiac expression levels of Bax and Cyto-C in the mice were visibly reduced under oral B307 treatment but were visibly enhanced under DOX treatment.

Negative Control:

Article Title: Para amino benzoic acid-derived self-assembled biocompatible nanoparticles for efficient delivery of siRNA
Article Snippet: RNeasy kits, QiaShredder spin columns, and negative control RNA were sourced from Qiagen (Hilden, Germany). .. Rabbit monoclonal primary antibody for Bcl-2 and mouse monoclonal antibody β-actin were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA) and Abcam (Cambridge, MA, USA), respectively.

Binding Assay:

Article Title: Melatonin Treatment Regulates SIRT3 Expression in Early Brain Injury (EBI) Due to Reactive Oxygen Species (ROS) in a Mouse Model of Subarachnoid Hemorrhage (SAH)
Article Snippet: The samples were then separated using 8–12% SDS-polyacrylamide gel electrophoresis (PAGE) and transferred to nitrocellulose membranes (Amersham Biosciences, Piscataway, NJ, USA), then incubated at 37 °C for 60 min in a Tris-buffered saline (TBS) containing 10% nonfat dried milk powder and 0.1% Tween20 to eliminate nonspecific antibody binding. .. The nitrocellulose membranes were incubated with the primary antibodies to Sirt3, Bax, Bcl-2, superoxide dismutase (SOD), and cleaved caspase-3 (1: 4,000 dilution) (Santa Cruz, Biotech) and a primary antibody against β-actin (1: 8,000 dilution, Santa Cruz, Biotech) for 12 hours at 4°C, followed by two hours of incubation at room temperature with the secondary antibodies (1: 5,000 dilution) (Sigma-Aldrich Co., USA).

Lysis:

Article Title: Melatonin Treatment Regulates SIRT3 Expression in Early Brain Injury (EBI) Due to Reactive Oxygen Species (ROS) in a Mouse Model of Subarachnoid Hemorrhage (SAH)
Article Snippet: The U87 and U251 cells were washed twice using ice-cold phosphate-buffered saline (PBS) before being lysed in RIPA lysis buffer containing 150 mM NaCl, 50 mM Tris-HCl (pH 7.4), 1% NP-40, 0.1% sodium dodecyl sulfate (SDS) and protease inhibitors (Roche, Diagnostics, Indianapolis, IN, USA). .. The nitrocellulose membranes were incubated with the primary antibodies to Sirt3, Bax, Bcl-2, superoxide dismutase (SOD), and cleaved caspase-3 (1: 4,000 dilution) (Santa Cruz, Biotech) and a primary antibody against β-actin (1: 8,000 dilution, Santa Cruz, Biotech) for 12 hours at 4°C, followed by two hours of incubation at room temperature with the secondary antibodies (1: 5,000 dilution) (Sigma-Aldrich Co., USA).

Article Title: JARID1B deletion induced apoptosis in Jeko-1 and HL-60 cell lines
Article Snippet: After incubation, total proteins were prepared from each culture condition with a lysis buffer containing freshly prepared protease inhibitors. .. Membranes were incubated with monoclonal anti-tri-methylated-histoneH3K4, anti-histone acetylation of H3, H4, JARID1B (Upstate, UAS), BCL-2, proaspase-3, C-myc, cyclin D1 (Santa Cruz USA).

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    Santa Cruz Biotechnology bcl 2
    NaN 3 induces mitochondria-mediated apoptosis through the expression of Pgc-1α-associated proteins in PC12 cells. (A) Expression levels of Pgc-1α, Nrf-1, Nrf-2, Tfam and Cox IV detected by western blot analysis. (B) Expression levels of procaspase-3, Bax, <t>Bcl-2</t> and cyt-c detected by western blot analysis. (C) Expression levels of pan-calcineurin A, CaMKII, p-CaMKII, p38 MAPK, p-p38 MAPK, Erk1/2 and p-Erk1/2 detected by western blot analysis. β-actin and GAPDH were used as the internal control. Band intensity ratios for each group are presented as mean ± standard deviation (n=3). *P
    Bcl 2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 99/100, based on 589 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    NaN 3 induces mitochondria-mediated apoptosis through the expression of Pgc-1α-associated proteins in PC12 cells. (A) Expression levels of Pgc-1α, Nrf-1, Nrf-2, Tfam and Cox IV detected by western blot analysis. (B) Expression levels of procaspase-3, Bax, Bcl-2 and cyt-c detected by western blot analysis. (C) Expression levels of pan-calcineurin A, CaMKII, p-CaMKII, p38 MAPK, p-p38 MAPK, Erk1/2 and p-Erk1/2 detected by western blot analysis. β-actin and GAPDH were used as the internal control. Band intensity ratios for each group are presented as mean ± standard deviation (n=3). *P

    Journal: Molecular Medicine Reports

    Article Title: Sodium azide induces mitochondria-mediated apoptosis in PC12 cells through Pgc-1α-associated signaling pathway

    doi: 10.3892/mmr.2019.9853

    Figure Lengend Snippet: NaN 3 induces mitochondria-mediated apoptosis through the expression of Pgc-1α-associated proteins in PC12 cells. (A) Expression levels of Pgc-1α, Nrf-1, Nrf-2, Tfam and Cox IV detected by western blot analysis. (B) Expression levels of procaspase-3, Bax, Bcl-2 and cyt-c detected by western blot analysis. (C) Expression levels of pan-calcineurin A, CaMKII, p-CaMKII, p38 MAPK, p-p38 MAPK, Erk1/2 and p-Erk1/2 detected by western blot analysis. β-actin and GAPDH were used as the internal control. Band intensity ratios for each group are presented as mean ± standard deviation (n=3). *P

    Article Snippet: Following blocking with 5% bovine serum albumin in TBS containing 0.1% Tween-20 (TBST) for 2 h at room temperature, the membranes were incubated with primary antibodies against Pgc-1α (Abcam, Cambridge, MA, USA; 1:500), Nrf-2 (Abcam; 1:500), Cox IV (Abcam; 1:1,000), Tfam (Abcam; 1:1,000), procaspase-3 (Abcam; 1:500), Nrf-1 (Cell Signaling Technology, Inc., Danvers, MA, USA, 1:500), pan-calcineurin A (CaN; Cell Signaling Technology Inc.; 1:1,000), phosphorylated (p)-CaMKII (Cell Signaling Technology; 1:1,000), p-p38 MAPK (Cell Signaling Technology, Inc.; 1:1,000), p-extracellular signal-regulated kinase (Erk)1/2 (Cell Signaling Technology, Inc.; 1:1,000), B-cell lymphoma-2 (Bcl-2)-associated X protein (Bax; Santa Cruz Biotechnology, Inc., Dallas, TX, USA; 1:200), Bcl-2 (Santa Cruz Biotechnology, Inc.; 1:200) and cytochrome c (Santa Cruz Biotechnology, Inc.; 1:200) at 4°C overnight.

    Techniques: Expressing, Pyrolysis Gas Chromatography, Western Blot, Standard Deviation

    Effect of K36 on UVA-induced Bcl-2 expression in human epidermal keratinocytes. The representative image of the western blot ( a ) and the average value of the triplicate experiment ( b ); significant difference versus nonirradiated group: ###, p

    Journal: International Journal of Molecular Sciences

    Article Title: Protective Effects and Mechanisms of N-Phenethyl Caffeamide from UVA-Induced Skin Damage in Human Epidermal Keratinocytes through Nrf2/HO-1 Regulation

    doi: 10.3390/ijms20010164

    Figure Lengend Snippet: Effect of K36 on UVA-induced Bcl-2 expression in human epidermal keratinocytes. The representative image of the western blot ( a ) and the average value of the triplicate experiment ( b ); significant difference versus nonirradiated group: ###, p

    Article Snippet: ERK-1 (sc-93), MMP-1 (sc-12348), MMP-2 (sc-13595), Bcl-2 (sc-7382), c-Fos (sc-7202), COX-2 (sc-19999), JNK (sc-46006), and β-Actin (sc-1616) were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

    Techniques: Expressing, Western Blot

    Effect of hesperidin on the expression of Bcl-2, caspase-3, TLR-4, and HSP70 protein in the lung tissue of CLP-induced lung injury mice. Mean ±SEM (n=6). ## p

    Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

    Article Title: Protective Effect of Hesperidin Against Sepsis-Induced Lung Injury by Inducing the Heat-Stable Protein 70 (Hsp70)/Toll-Like Receptor 4 (TLR4)/ Myeloid Differentiation Primary Response 88 (MyD88) Pathway

    doi: 10.12659/MSM.912490

    Figure Lengend Snippet: Effect of hesperidin on the expression of Bcl-2, caspase-3, TLR-4, and HSP70 protein in the lung tissue of CLP-induced lung injury mice. Mean ±SEM (n=6). ## p

    Article Snippet: Proteins were transferred onto nitrocellulose membranes and incubated overnight with caspase-3 (1: 500), Bcl-2 (1: 1000), TLR4 (1: 1000), Hsp70 (1: 1000), and β-Actin antibody (Santa Cruz Biotechnology Inc., Santa Cruz, USA).

    Techniques: Expressing, Mouse Assay

    Effect of bergenin at indicated concentrations on the expression of Bax and Bcl-2 proteins in HeLa cells as shown in the western blot. The experiments were carried out in triplicates. The values were considered significant at *P

    Journal: Experimental and Therapeutic Medicine

    Article Title: Anticancer activity of bergenin against cervical cancer cells involves apoptosis, cell cycle arrest, inhibition of cell migration and the STAT3 signalling pathway

    doi: 10.3892/etm.2019.7380

    Figure Lengend Snippet: Effect of bergenin at indicated concentrations on the expression of Bax and Bcl-2 proteins in HeLa cells as shown in the western blot. The experiments were carried out in triplicates. The values were considered significant at *P

    Article Snippet: Afterwards, blocking was done with 5% non-fat milk followed by an incubation at RT for 1 h. The membranes were then subjected to treatment either specific primary antibody (STAT3; cat. no. sc-293151, p-STAT3 (Ser 727); cat. no. sc-8001-R, p-STAT (Tyr705); cat. no. sc-7993-R, Bax; cat. no. sc-20067, Bcl-2; sc-509, Actin; sc-58673 purchased from Santa Cruz Biotechnology Inc.) at 4°C for 20 h. Thereafter, washing in washing buffer was carried out and then the membranes were incubated with secondery antibody (mouse monoclonal secondary antibody conjugated to Horseradish Peroxidase, cat. no. sc-2357) for 1 h. The protein bands were then visualised by an ECL Advanced Western Blot Detection kit.

    Techniques: Expressing, Western Blot