pro-survival proteins survivin Search Results


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  • 99
    Millipore ϐ actin
    ϐ Actin, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    88
    SMAC Corp pro apoptotic proteins
    Pro Apoptotic Proteins, supplied by SMAC Corp, used in various techniques. Bioz Stars score: 88/100, based on 45 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti apoptotic
    Immunoblot detection of prostate cancer cells targeted by using PBM nanoparticle and the expression of pro- and <t>anti-apoptotic,</t> pro-survival and proliferation markers
    Anti Apoptotic, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam α7 nachr
    Immunoblot detection of prostate cancer cells targeted by using PBM nanoparticle and the expression of pro- and <t>anti-apoptotic,</t> pro-survival and proliferation markers
    α7 Nachr, supplied by Abcam, used in various techniques. Bioz Stars score: 92/100, based on 104 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Santa Cruz Biotechnology c iap1
    The expression of <t>c-IAP1,</t> Bcl-2, Bcl-xl, survivin and PARP in A2780 and C200 cells . Cells untreated or treated with 10 or 25 μM genistein (Gen), 250 nM cisplatin (Cis), the combination (Gen + Cis), 1 or 2 nM taxotere (Tax), the combination (Gen + Tax), 2 or 50 nM gemcitabine (Gem) and the combination (Gen + Gem). β-actin antibodies were used as internal controls for equal loading of proteins. Significant down-regulation of c-IAP1, Bcl-2, Bcl-xl, survivin and PARP was observed in A2780 and C200 cells treated with the combination of genistein and either cisplatin, gemcitabine or taxotere compared to cells treated with either drug alone.
    C Iap1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 91/100, based on 45 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc iap family antibody sampler kit
    The expression of <t>c-IAP1,</t> Bcl-2, Bcl-xl, survivin and PARP in A2780 and C200 cells . Cells untreated or treated with 10 or 25 μM genistein (Gen), 250 nM cisplatin (Cis), the combination (Gen + Cis), 1 or 2 nM taxotere (Tax), the combination (Gen + Tax), 2 or 50 nM gemcitabine (Gem) and the combination (Gen + Gem). β-actin antibodies were used as internal controls for equal loading of proteins. Significant down-regulation of c-IAP1, Bcl-2, Bcl-xl, survivin and PARP was observed in A2780 and C200 cells treated with the combination of genistein and either cisplatin, gemcitabine or taxotere compared to cells treated with either drug alone.
    Iap Family Antibody Sampler Kit, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 91/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Santa Cruz Biotechnology cleaved caspase 3
    The expression of <t>c-IAP1,</t> Bcl-2, Bcl-xl, survivin and PARP in A2780 and C200 cells . Cells untreated or treated with 10 or 25 μM genistein (Gen), 250 nM cisplatin (Cis), the combination (Gen + Cis), 1 or 2 nM taxotere (Tax), the combination (Gen + Tax), 2 or 50 nM gemcitabine (Gem) and the combination (Gen + Gem). β-actin antibodies were used as internal controls for equal loading of proteins. Significant down-regulation of c-IAP1, Bcl-2, Bcl-xl, survivin and PARP was observed in A2780 and C200 cells treated with the combination of genistein and either cisplatin, gemcitabine or taxotere compared to cells treated with either drug alone.
    Cleaved Caspase 3, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1672 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Mimetics ciap1 2
    TNFα-mediated transient IKK activation pathways. (A) Signaling pathways to full IKK activation. Upon ligation, TNFR1 recruits TRADD, RIP1, TRAF2, and <t>cIAP1/2.</t> TRAF2 and cIAP1/2, in conjunction with UbcH5, catalyze RIP1 ubiquitination through linear (M1-pUb) and K63 linkages (K63-pUb), and also undergo autoubiquitination through K63-linkage. K63-pUb recruits the TAK1-TAB1-TAB2 complex, and M1-pUb recruits the IKKα-IKKβ-NEMO complex, leading to TAK1-mediated activation of the early phase of IKK. Thereafter, K63-pUb recruits the HOIL-1L–HOIP complex, which in turn recruits and catalyzes linear ubiquitination of NEMO, leading to more IKK recruitment and full activation of IKK. Such full IKK activation is required for the efficient expression of NF-κB target genes. (B) RIP1-independent pathway to delayed IKK activation. RIP1 protein is not detectable in embryonic hepatocytes. As a result, upon TNFR1 ligation, receptor-recruited TRAF2 and cIAP1/2 undergo increased autoubiquitination through K63 and K48 linkages. The K63-pUb chains then recruit the TAK1-TAB1-TAB2 and HOIP–HOIL-1 complexes, leading to activation of the delayed phase of IKK. Such delayed IKK activation is sufficient for induction of some NF-κB target genes (e.g., IκBα and IP-10).
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    Cell Signaling Technology Inc mmp2
    TNFα-mediated transient IKK activation pathways. (A) Signaling pathways to full IKK activation. Upon ligation, TNFR1 recruits TRADD, RIP1, TRAF2, and <t>cIAP1/2.</t> TRAF2 and cIAP1/2, in conjunction with UbcH5, catalyze RIP1 ubiquitination through linear (M1-pUb) and K63 linkages (K63-pUb), and also undergo autoubiquitination through K63-linkage. K63-pUb recruits the TAK1-TAB1-TAB2 complex, and M1-pUb recruits the IKKα-IKKβ-NEMO complex, leading to TAK1-mediated activation of the early phase of IKK. Thereafter, K63-pUb recruits the HOIL-1L–HOIP complex, which in turn recruits and catalyzes linear ubiquitination of NEMO, leading to more IKK recruitment and full activation of IKK. Such full IKK activation is required for the efficient expression of NF-κB target genes. (B) RIP1-independent pathway to delayed IKK activation. RIP1 protein is not detectable in embryonic hepatocytes. As a result, upon TNFR1 ligation, receptor-recruited TRAF2 and cIAP1/2 undergo increased autoubiquitination through K63 and K48 linkages. The K63-pUb chains then recruit the TAK1-TAB1-TAB2 and HOIP–HOIL-1 complexes, leading to activation of the delayed phase of IKK. Such delayed IKK activation is sufficient for induction of some NF-κB target genes (e.g., IκBα and IP-10).
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    Santa Cruz Biotechnology pro caspase 3
    TNFα-mediated transient IKK activation pathways. (A) Signaling pathways to full IKK activation. Upon ligation, TNFR1 recruits TRADD, RIP1, TRAF2, and <t>cIAP1/2.</t> TRAF2 and cIAP1/2, in conjunction with UbcH5, catalyze RIP1 ubiquitination through linear (M1-pUb) and K63 linkages (K63-pUb), and also undergo autoubiquitination through K63-linkage. K63-pUb recruits the TAK1-TAB1-TAB2 complex, and M1-pUb recruits the IKKα-IKKβ-NEMO complex, leading to TAK1-mediated activation of the early phase of IKK. Thereafter, K63-pUb recruits the HOIL-1L–HOIP complex, which in turn recruits and catalyzes linear ubiquitination of NEMO, leading to more IKK recruitment and full activation of IKK. Such full IKK activation is required for the efficient expression of NF-κB target genes. (B) RIP1-independent pathway to delayed IKK activation. RIP1 protein is not detectable in embryonic hepatocytes. As a result, upon TNFR1 ligation, receptor-recruited TRAF2 and cIAP1/2 undergo increased autoubiquitination through K63 and K48 linkages. The K63-pUb chains then recruit the TAK1-TAB1-TAB2 and HOIP–HOIL-1 complexes, leading to activation of the delayed phase of IKK. Such delayed IKK activation is sufficient for induction of some NF-κB target genes (e.g., IκBα and IP-10).
    Pro Caspase 3, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 218 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    GeneTex cyclin a2
    p-Akt and p-NFκB levels of C 2 -ceramide-treated H1299 lung cancer cells. Cells treated with different concentrations (0 to 50 μM) of C 2 -ceramide for 24 h. After treatment, the protein lysates were resolved by SDS-PAGE, transferred onto nitrocellulose membranes and probed with specific antibodies and detected signals using an enhanced chemiluminescence kit. (a) The changes of Akt and NFκB phosphorylation. (b) The changes of protein level of survivin, <t>cyclin</t> A2 and Bax. β-actin as an internal control.
    Cyclin A2, supplied by GeneTex, used in various techniques. Bioz Stars score: 92/100, based on 23 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology antibodies against p27
    p-Akt and p-NFκB levels of C 2 -ceramide-treated H1299 lung cancer cells. Cells treated with different concentrations (0 to 50 μM) of C 2 -ceramide for 24 h. After treatment, the protein lysates were resolved by SDS-PAGE, transferred onto nitrocellulose membranes and probed with specific antibodies and detected signals using an enhanced chemiluminescence kit. (a) The changes of Akt and NFκB phosphorylation. (b) The changes of protein level of survivin, <t>cyclin</t> A2 and Bax. β-actin as an internal control.
    Antibodies Against P27, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 88/100, based on 46 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc cleaved parp
    p-Akt and p-NFκB levels of C 2 -ceramide-treated H1299 lung cancer cells. Cells treated with different concentrations (0 to 50 μM) of C 2 -ceramide for 24 h. After treatment, the protein lysates were resolved by SDS-PAGE, transferred onto nitrocellulose membranes and probed with specific antibodies and detected signals using an enhanced chemiluminescence kit. (a) The changes of Akt and NFκB phosphorylation. (b) The changes of protein level of survivin, <t>cyclin</t> A2 and Bax. β-actin as an internal control.
    Cleaved Parp, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 7715 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cytoskeleton Inc cytoskeleton spindle microtubules
    p-Akt and p-NFκB levels of C 2 -ceramide-treated H1299 lung cancer cells. Cells treated with different concentrations (0 to 50 μM) of C 2 -ceramide for 24 h. After treatment, the protein lysates were resolved by SDS-PAGE, transferred onto nitrocellulose membranes and probed with specific antibodies and detected signals using an enhanced chemiluminescence kit. (a) The changes of Akt and NFκB phosphorylation. (b) The changes of protein level of survivin, <t>cyclin</t> A2 and Bax. β-actin as an internal control.
    Cytoskeleton Spindle Microtubules, supplied by Cytoskeleton Inc, used in various techniques. Bioz Stars score: 85/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    95
    Millipore bcl 2
    The expression of c-IAP1, <t>Bcl-2,</t> Bcl-xl, survivin and PARP in A2780 and C200 cells . Cells untreated or treated with 10 or 25 μM genistein (Gen), 250 nM cisplatin (Cis), the combination (Gen + Cis), 1 or 2 nM taxotere (Tax), the combination (Gen + Tax), 2 or 50 nM gemcitabine (Gem) and the combination (Gen + Gem). β-actin antibodies were used as internal controls for equal loading of proteins. Significant down-regulation of c-IAP1, Bcl-2, Bcl-xl, survivin and PARP was observed in A2780 and C200 cells treated with the combination of genistein and either cisplatin, gemcitabine or taxotere compared to cells treated with either drug alone.
    Bcl 2, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 1869 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology dkk1
    JNK is required for Ischemia-Induced Elevation of <t>Dkk1</t> and Loss of Survivin in Long-Term Estrogen-Deprived Female Rats
    Dkk1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 208 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc sirt1
    Illustrative model of the action of liraglutide on the infarcted heart via Parkin-dependent mitophagy, through the activation of <t>SIRT1.</t> Liraglutide signals SIRT1 which enhances the expression of Parkin, the receptor of mitophagy. Through the SIRT1/Parkin pathway, liraglutide activates mitophagy which is vital for the improvement of the infarcted heart. Protective mitophagy blocks mitochondrial apoptosis, promoting cardiomyocyte survival. In addition, mitophagy alleviates oxidative stress and preserves the mitochondrial function. These beneficial effects reduce cardiac fibrosis and the inflammatory responses, leading to the improvement of the infarcted heart. SIRT1, NAD-dependent protein deacetylase sirtuin-1.
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    Abcam cyclin d1
    Illustrative model of the action of liraglutide on the infarcted heart via Parkin-dependent mitophagy, through the activation of <t>SIRT1.</t> Liraglutide signals SIRT1 which enhances the expression of Parkin, the receptor of mitophagy. Through the SIRT1/Parkin pathway, liraglutide activates mitophagy which is vital for the improvement of the infarcted heart. Protective mitophagy blocks mitochondrial apoptosis, promoting cardiomyocyte survival. In addition, mitophagy alleviates oxidative stress and preserves the mitochondrial function. These beneficial effects reduce cardiac fibrosis and the inflammatory responses, leading to the improvement of the infarcted heart. SIRT1, NAD-dependent protein deacetylase sirtuin-1.
    Cyclin D1, supplied by Abcam, used in various techniques. Bioz Stars score: 94/100, based on 2883 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    97
    R&D Systems caspase 3
    Immunocytochemistry showed that <t>caspase-3</t> was activated. The shrunken cells were positively stained for activated caspase-3. No positive cell was detectable in the control group ( A: original magnification, × 200). Whereas large numbers of positive cells labeled for activated caspase-3 were observed in HepG2 cells treated with 30 μmol/L troglitazone for 24 h ( B: original magnification, × 400).
    Caspase 3, supplied by R&D Systems, used in various techniques. Bioz Stars score: 97/100, based on 1282 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc bax
    Inhibitory effect of combined treatment with BAI and GEM on the proliferation of the human CFPAC-1 pancreatic cancer cell line in vivo . Representative images of (A) mice and (B) tumors. (C) Tumor volume changes in the xenografts. Resected tumors revealed that combination therapy decreased the tumor volume significantly compared with either the control group or the BAI-alone treated group. The data are presented as the mean ± SEM. (D) Following 28 days of treatment, the tumor weights were significantly decreased in all 3 treatment groups compared with the control group. The data are presented as the mean ± SEM. Representative immunohistochemical staining images and quantification for (E) <t>Bcl-2,</t> (F) <t>Bax,</t> (G) caspase-3 and (H) survivin from all groups of mice following treatment with BAI alone, GEM alone or a combination of the 2 treatments. Images were captured using a light microscope at a magnification of ×20. **P
    Bax, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 13298 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc bik
    Tumor cell apoptosis is induced by AdC7-SP/E1A-ΔE3 via a <t>p53-independent</t> mitochondrial pathway NCI-H508 and Huh7 cells were infected at 100 MOI with AdC7-ΔE1-ΔE3, AdC7-ΔE3, and AdC7-SP/E1A-ΔE3. NCI-H508 cells were collected at 12 h and 24 h post infection, and Huh7 cells were collected 24 h and 48 h post-infection. Western blotting was carried out to detect levels of p53, phosphorylation of p53, MCL-1, Bcl-2, Bcl-xl, <t>Bik</t> and phosphorylation of Bad in NCI-H508 and Huh7 cells. β-actin was used as a loading control.
    Bik, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 174 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti rip
    Tumor cell apoptosis is induced by AdC7-SP/E1A-ΔE3 via a <t>p53-independent</t> mitochondrial pathway NCI-H508 and Huh7 cells were infected at 100 MOI with AdC7-ΔE1-ΔE3, AdC7-ΔE3, and AdC7-SP/E1A-ΔE3. NCI-H508 cells were collected at 12 h and 24 h post infection, and Huh7 cells were collected 24 h and 48 h post-infection. Western blotting was carried out to detect levels of p53, phosphorylation of p53, MCL-1, Bcl-2, Bcl-xl, <t>Bik</t> and phosphorylation of Bad in NCI-H508 and Huh7 cells. β-actin was used as a loading control.
    Anti Rip, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Charles River Laboratories pai 1
    Tumor cell apoptosis is induced by AdC7-SP/E1A-ΔE3 via a <t>p53-independent</t> mitochondrial pathway NCI-H508 and Huh7 cells were infected at 100 MOI with AdC7-ΔE1-ΔE3, AdC7-ΔE3, and AdC7-SP/E1A-ΔE3. NCI-H508 cells were collected at 12 h and 24 h post infection, and Huh7 cells were collected 24 h and 48 h post-infection. Western blotting was carried out to detect levels of p53, phosphorylation of p53, MCL-1, Bcl-2, Bcl-xl, <t>Bik</t> and phosphorylation of Bad in NCI-H508 and Huh7 cells. β-actin was used as a loading control.
    Pai 1, supplied by Charles River Laboratories, used in various techniques. Bioz Stars score: 92/100, based on 205 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc bcl 2
    Tumor cell apoptosis is induced by AdC7-SP/E1A-ΔE3 via a <t>p53-independent</t> mitochondrial pathway NCI-H508 and Huh7 cells were infected at 100 MOI with AdC7-ΔE1-ΔE3, AdC7-ΔE3, and AdC7-SP/E1A-ΔE3. NCI-H508 cells were collected at 12 h and 24 h post infection, and Huh7 cells were collected 24 h and 48 h post-infection. Western blotting was carried out to detect levels of p53, phosphorylation of p53, MCL-1, Bcl-2, Bcl-xl, <t>Bik</t> and phosphorylation of Bad in NCI-H508 and Huh7 cells. β-actin was used as a loading control.
    Bcl 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 16873 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Immunoblot detection of prostate cancer cells targeted by using PBM nanoparticle and the expression of pro- and anti-apoptotic, pro-survival and proliferation markers

    Journal: Cancer letters

    Article Title: Reversal of drug resistance by planetary ball milled (PBM) nanoparticle loaded with resveratrol and docetaxel in prostate cancer

    doi: 10.1016/j.canlet.2018.04.017

    Figure Lengend Snippet: Immunoblot detection of prostate cancer cells targeted by using PBM nanoparticle and the expression of pro- and anti-apoptotic, pro-survival and proliferation markers

    Article Snippet: The primary and secondary antibody for pro-apoptotic (BAX, BAK), Cleaved Caspase-3, anti-apoptotic (BCL-2, BCL-XL, Survivin), NF-kB p65, COX-2, GAPDH, ABCB1, ABCC1, ABCG2, were procured from Cell Signaling Technology (MA, USA).

    Techniques: Expressing

    The expression of c-IAP1, Bcl-2, Bcl-xl, survivin and PARP in A2780 and C200 cells . Cells untreated or treated with 10 or 25 μM genistein (Gen), 250 nM cisplatin (Cis), the combination (Gen + Cis), 1 or 2 nM taxotere (Tax), the combination (Gen + Tax), 2 or 50 nM gemcitabine (Gem) and the combination (Gen + Gem). β-actin antibodies were used as internal controls for equal loading of proteins. Significant down-regulation of c-IAP1, Bcl-2, Bcl-xl, survivin and PARP was observed in A2780 and C200 cells treated with the combination of genistein and either cisplatin, gemcitabine or taxotere compared to cells treated with either drug alone.

    Journal: Journal of Ovarian Research

    Article Title: Sensitization of ovarian cancer cells to cisplatin by genistein: the role of NF-kappaB

    doi: 10.1186/1757-2215-1-9

    Figure Lengend Snippet: The expression of c-IAP1, Bcl-2, Bcl-xl, survivin and PARP in A2780 and C200 cells . Cells untreated or treated with 10 or 25 μM genistein (Gen), 250 nM cisplatin (Cis), the combination (Gen + Cis), 1 or 2 nM taxotere (Tax), the combination (Gen + Tax), 2 or 50 nM gemcitabine (Gem) and the combination (Gen + Gem). β-actin antibodies were used as internal controls for equal loading of proteins. Significant down-regulation of c-IAP1, Bcl-2, Bcl-xl, survivin and PARP was observed in A2780 and C200 cells treated with the combination of genistein and either cisplatin, gemcitabine or taxotere compared to cells treated with either drug alone.

    Article Snippet: The induction of apoptotic cell death could in part be due to inactivation of important survival genes; and therefore the expressions of pro-survival and anti-apoptotic molecules such as survivin, Bcl-2, Bcl-xL, and c-IAP1, which are transcriptionally regulated by NF-κB, were also evaluated.

    Techniques: Expressing

    TNFα-mediated transient IKK activation pathways. (A) Signaling pathways to full IKK activation. Upon ligation, TNFR1 recruits TRADD, RIP1, TRAF2, and cIAP1/2. TRAF2 and cIAP1/2, in conjunction with UbcH5, catalyze RIP1 ubiquitination through linear (M1-pUb) and K63 linkages (K63-pUb), and also undergo autoubiquitination through K63-linkage. K63-pUb recruits the TAK1-TAB1-TAB2 complex, and M1-pUb recruits the IKKα-IKKβ-NEMO complex, leading to TAK1-mediated activation of the early phase of IKK. Thereafter, K63-pUb recruits the HOIL-1L–HOIP complex, which in turn recruits and catalyzes linear ubiquitination of NEMO, leading to more IKK recruitment and full activation of IKK. Such full IKK activation is required for the efficient expression of NF-κB target genes. (B) RIP1-independent pathway to delayed IKK activation. RIP1 protein is not detectable in embryonic hepatocytes. As a result, upon TNFR1 ligation, receptor-recruited TRAF2 and cIAP1/2 undergo increased autoubiquitination through K63 and K48 linkages. The K63-pUb chains then recruit the TAK1-TAB1-TAB2 and HOIP–HOIL-1 complexes, leading to activation of the delayed phase of IKK. Such delayed IKK activation is sufficient for induction of some NF-κB target genes (e.g., IκBα and IP-10).

    Journal: Cellular signalling

    Article Title: TNFR1 Signaling Kinetics: Spatiotemporal Control of Three Phases of IKK activation by Posttranslational Modification

    doi: 10.1016/j.cellsig.2013.04.005

    Figure Lengend Snippet: TNFα-mediated transient IKK activation pathways. (A) Signaling pathways to full IKK activation. Upon ligation, TNFR1 recruits TRADD, RIP1, TRAF2, and cIAP1/2. TRAF2 and cIAP1/2, in conjunction with UbcH5, catalyze RIP1 ubiquitination through linear (M1-pUb) and K63 linkages (K63-pUb), and also undergo autoubiquitination through K63-linkage. K63-pUb recruits the TAK1-TAB1-TAB2 complex, and M1-pUb recruits the IKKα-IKKβ-NEMO complex, leading to TAK1-mediated activation of the early phase of IKK. Thereafter, K63-pUb recruits the HOIL-1L–HOIP complex, which in turn recruits and catalyzes linear ubiquitination of NEMO, leading to more IKK recruitment and full activation of IKK. Such full IKK activation is required for the efficient expression of NF-κB target genes. (B) RIP1-independent pathway to delayed IKK activation. RIP1 protein is not detectable in embryonic hepatocytes. As a result, upon TNFR1 ligation, receptor-recruited TRAF2 and cIAP1/2 undergo increased autoubiquitination through K63 and K48 linkages. The K63-pUb chains then recruit the TAK1-TAB1-TAB2 and HOIP–HOIL-1 complexes, leading to activation of the delayed phase of IKK. Such delayed IKK activation is sufficient for induction of some NF-κB target genes (e.g., IκBα and IP-10).

    Article Snippet: In addition, NF-κB activation induces the expression of cIAP1/2, Bcl-XL, survivin and cFLIP, and these pro-survival proteins then confer upon cancer cells the ability to survive and adapt to stressful tumor microenvironments characterized by hypoxia, hypoglycemia, and the increased production of free radicals – conditions that potentiate chronic inflammation and oxidative stress [ , ].

    Techniques: Activation Assay, Ligation, Expressing

    Crosstalk in TNFR1 signaling. Ligation of TNFR1 leads to activation of the pro-inflammatory NF-κB and JNK, and pro-apoptotic caspase-8 and ROS pathways. However, in normal cells, NF-κB target gene products suppress pro-apoptotic pathways. For instance, cIAP1/2 and cFLIP inhibit caspase-8 activation, XIAP and GADD45β suppress prolonged JNK activation, and FHC and Mn-SOD inhibit ROS accumulation. Therefore, unless NF-κB pathway is blocked, TNFα is insufficient to induce cell death.

    Journal: Cellular signalling

    Article Title: TNFR1 Signaling Kinetics: Spatiotemporal Control of Three Phases of IKK activation by Posttranslational Modification

    doi: 10.1016/j.cellsig.2013.04.005

    Figure Lengend Snippet: Crosstalk in TNFR1 signaling. Ligation of TNFR1 leads to activation of the pro-inflammatory NF-κB and JNK, and pro-apoptotic caspase-8 and ROS pathways. However, in normal cells, NF-κB target gene products suppress pro-apoptotic pathways. For instance, cIAP1/2 and cFLIP inhibit caspase-8 activation, XIAP and GADD45β suppress prolonged JNK activation, and FHC and Mn-SOD inhibit ROS accumulation. Therefore, unless NF-κB pathway is blocked, TNFα is insufficient to induce cell death.

    Article Snippet: In addition, NF-κB activation induces the expression of cIAP1/2, Bcl-XL, survivin and cFLIP, and these pro-survival proteins then confer upon cancer cells the ability to survive and adapt to stressful tumor microenvironments characterized by hypoxia, hypoglycemia, and the increased production of free radicals – conditions that potentiate chronic inflammation and oxidative stress [ , ].

    Techniques: Ligation, Activation Assay

    p-Akt and p-NFκB levels of C 2 -ceramide-treated H1299 lung cancer cells. Cells treated with different concentrations (0 to 50 μM) of C 2 -ceramide for 24 h. After treatment, the protein lysates were resolved by SDS-PAGE, transferred onto nitrocellulose membranes and probed with specific antibodies and detected signals using an enhanced chemiluminescence kit. (a) The changes of Akt and NFκB phosphorylation. (b) The changes of protein level of survivin, cyclin A2 and Bax. β-actin as an internal control.

    Journal: Cancer Cell International

    Article Title: The antiproliferative effect of C2-ceramide on lung cancer cells through apoptosis by inhibiting Akt and NF?B

    doi: 10.1186/1475-2867-14-1

    Figure Lengend Snippet: p-Akt and p-NFκB levels of C 2 -ceramide-treated H1299 lung cancer cells. Cells treated with different concentrations (0 to 50 μM) of C 2 -ceramide for 24 h. After treatment, the protein lysates were resolved by SDS-PAGE, transferred onto nitrocellulose membranes and probed with specific antibodies and detected signals using an enhanced chemiluminescence kit. (a) The changes of Akt and NFκB phosphorylation. (b) The changes of protein level of survivin, cyclin A2 and Bax. β-actin as an internal control.

    Article Snippet: C2 -ceramide also reduces the pro-survival proteins Akt and NFκB, causing the down-regulation of survivin and cyclin A2, which are reported to frequently overexpress in non-small cell lung cancer [ ].

    Techniques: SDS Page

    Schematic diagram of hypothesized mechanism of C 2 -ceramide-induced apoptosis of lung cancer cells. C 2 -ceramide inhibits the activity of both Akt and NF-κB, causing the down-regulation of pro-survival survivin and cell cycle promoter cyclin A2. On the contrary, C 2 -ceramide increases the protein level of pro-apoptotic Bax. As a result, C 2 -creamide treatment causes cell cycle G 1 arrest and chromatin condensation, subsequently, triggering the apoptosis of lung cancer cells.

    Journal: Cancer Cell International

    Article Title: The antiproliferative effect of C2-ceramide on lung cancer cells through apoptosis by inhibiting Akt and NF?B

    doi: 10.1186/1475-2867-14-1

    Figure Lengend Snippet: Schematic diagram of hypothesized mechanism of C 2 -ceramide-induced apoptosis of lung cancer cells. C 2 -ceramide inhibits the activity of both Akt and NF-κB, causing the down-regulation of pro-survival survivin and cell cycle promoter cyclin A2. On the contrary, C 2 -ceramide increases the protein level of pro-apoptotic Bax. As a result, C 2 -creamide treatment causes cell cycle G 1 arrest and chromatin condensation, subsequently, triggering the apoptosis of lung cancer cells.

    Article Snippet: C2 -ceramide also reduces the pro-survival proteins Akt and NFκB, causing the down-regulation of survivin and cyclin A2, which are reported to frequently overexpress in non-small cell lung cancer [ ].

    Techniques: Activity Assay

    The expression of c-IAP1, Bcl-2, Bcl-xl, survivin and PARP in A2780 and C200 cells . Cells untreated or treated with 10 or 25 μM genistein (Gen), 250 nM cisplatin (Cis), the combination (Gen + Cis), 1 or 2 nM taxotere (Tax), the combination (Gen + Tax), 2 or 50 nM gemcitabine (Gem) and the combination (Gen + Gem). β-actin antibodies were used as internal controls for equal loading of proteins. Significant down-regulation of c-IAP1, Bcl-2, Bcl-xl, survivin and PARP was observed in A2780 and C200 cells treated with the combination of genistein and either cisplatin, gemcitabine or taxotere compared to cells treated with either drug alone.

    Journal: Journal of Ovarian Research

    Article Title: Sensitization of ovarian cancer cells to cisplatin by genistein: the role of NF-kappaB

    doi: 10.1186/1757-2215-1-9

    Figure Lengend Snippet: The expression of c-IAP1, Bcl-2, Bcl-xl, survivin and PARP in A2780 and C200 cells . Cells untreated or treated with 10 or 25 μM genistein (Gen), 250 nM cisplatin (Cis), the combination (Gen + Cis), 1 or 2 nM taxotere (Tax), the combination (Gen + Tax), 2 or 50 nM gemcitabine (Gem) and the combination (Gen + Gem). β-actin antibodies were used as internal controls for equal loading of proteins. Significant down-regulation of c-IAP1, Bcl-2, Bcl-xl, survivin and PARP was observed in A2780 and C200 cells treated with the combination of genistein and either cisplatin, gemcitabine or taxotere compared to cells treated with either drug alone.

    Article Snippet: Expression of Bcl-2, Bcl-xL, survivin, and c-IAP1 proteins were significantly reduced in cells treated with the combination compared to either agent alone in both A2780 and C200 cells.

    Techniques: Expressing

    JNK is required for Ischemia-Induced Elevation of Dkk1 and Loss of Survivin in Long-Term Estrogen-Deprived Female Rats

    Journal: Steroids

    Article Title: Long-Term Estrogen Deprivation Leads to Elevation of Dickkopf-1 and Dysregulation of Wnt/ -Catenin Signaling in Hippocampal CA1 Neurons

    doi: 10.1016/j.steroids.2012.11.004

    Figure Lengend Snippet: JNK is required for Ischemia-Induced Elevation of Dkk1 and Loss of Survivin in Long-Term Estrogen-Deprived Female Rats

    Article Snippet: Along these lines, the decrease in survivin observed in the current study is likely due to the fact that Dkk1, as a Wnt/β-catenin pathway antagonist, prevents expression of critical β- catenin pro-survival genes, such as survivin.

    Techniques:

    Long-Term Estrogen Deprivation Leads to Loss of Estradiol Suppression of Neurodegenerative Dkk1 in CA1 Hippocampal Neurons

    Journal: Steroids

    Article Title: Long-Term Estrogen Deprivation Leads to Elevation of Dickkopf-1 and Dysregulation of Wnt/ -Catenin Signaling in Hippocampal CA1 Neurons

    doi: 10.1016/j.steroids.2012.11.004

    Figure Lengend Snippet: Long-Term Estrogen Deprivation Leads to Loss of Estradiol Suppression of Neurodegenerative Dkk1 in CA1 Hippocampal Neurons

    Article Snippet: Along these lines, the decrease in survivin observed in the current study is likely due to the fact that Dkk1, as a Wnt/β-catenin pathway antagonist, prevents expression of critical β- catenin pro-survival genes, such as survivin.

    Techniques:

    Illustrative model of the action of liraglutide on the infarcted heart via Parkin-dependent mitophagy, through the activation of SIRT1. Liraglutide signals SIRT1 which enhances the expression of Parkin, the receptor of mitophagy. Through the SIRT1/Parkin pathway, liraglutide activates mitophagy which is vital for the improvement of the infarcted heart. Protective mitophagy blocks mitochondrial apoptosis, promoting cardiomyocyte survival. In addition, mitophagy alleviates oxidative stress and preserves the mitochondrial function. These beneficial effects reduce cardiac fibrosis and the inflammatory responses, leading to the improvement of the infarcted heart. SIRT1, NAD-dependent protein deacetylase sirtuin-1.

    Journal: Molecular Medicine Reports

    Article Title: Liraglutide repairs the infarcted heart: The role of the SIRT1/Parkin/mitophagy pathway

    doi: 10.3892/mmr.2018.8371

    Figure Lengend Snippet: Illustrative model of the action of liraglutide on the infarcted heart via Parkin-dependent mitophagy, through the activation of SIRT1. Liraglutide signals SIRT1 which enhances the expression of Parkin, the receptor of mitophagy. Through the SIRT1/Parkin pathway, liraglutide activates mitophagy which is vital for the improvement of the infarcted heart. Protective mitophagy blocks mitochondrial apoptosis, promoting cardiomyocyte survival. In addition, mitophagy alleviates oxidative stress and preserves the mitochondrial function. These beneficial effects reduce cardiac fibrosis and the inflammatory responses, leading to the improvement of the infarcted heart. SIRT1, NAD-dependent protein deacetylase sirtuin-1.

    Article Snippet: The primaries antibodies used in the present study were against the following proteins: Pro-caspase3 (1:1,000; Cell Signaling Technology, Inc.; cat. no. 9662), cleaved caspase3 (1:1,000; Cell Signaling Technology, Inc.; cat. no. 9664), baculoviral IAP repeat-containing protein 2 (c-IAP1; 1:2,000; Cell Signaling Technology, Inc. cat. no. 7065), caspase9 (1:1,000; Abcam; cat. no. ab32539), Parkin (1:1,000; Cell Signaling Technology, Inc.; cat. no. 2132), microtubule-associated protein light chain (LC) 3II (1:1,000; Cell Signaling Technology, Inc.; cat. no. 3868), sequestome-1 (p62; 1:1,000; Abcam; cat. no. ab56416), Beclin1 (1:1,000; Cell Signaling Technology, Inc.; cat. no. 3495), autophagy protein 5 (Atg5; 1:1,000; Cell Signaling Technology, Inc.; cat. no. 12,994), Sirt1 (1:1,000; Cell Signaling Technology, Inc., cat. no. 9475), TGFβ (1:1,000; Cell Signaling Technology, Inc.; cat. no. 3711), matrix metalloproteinase (MMP) 9 (1:1,000; Cell Signaling Technology, Inc.; cat. no. 13667) and poly (ADP ribose) polymerase 1 (PARP; 1:1,000; Cell Signaling Technology, Inc.; cat. no. 9532) The mean densities of the bands were represented as the optical density in units/mm2 and normalized to that of β -actin (Quantity One, version 4.6.2; Bio-Rad Laboratories, Inc.).

    Techniques: Activation Assay, Expressing, Histone Deacetylase Assay

    Liraglutide activates Parkin via the SIRT1 pathway. (A) Western blotting and (B) densitometric analysis was used to detect the alterations in SIRT1 in the infarcted heart. Liraglutide was able to sustain the expression level of SIRT1 in a dose-dependent manner. In vitro , total proteins were isolated and analyzed via (C) western blotting to measure the alterations in (D) SIRT1 and (E) Parkin expression. SRT, the activator of SIRT1, was applied in the control group under hypoxia conditions. SRT elevated the expression levels of SIRT1 and Parkin in the context of hypoxic stimulation. Selisistat, the inhibitor of SIRT1, was used in the liraglutide-treated cells. Selisistat blocked the promotive effect of liraglutide on SIRT1 and Parkin expression. (F) Caspase9 activity and (G) LDH release assays were used to detect cell viability and mitochondrial apoptosis, respectively. (H) Co-staining of SIRT1 and Parkin. Liraglutide enhanced the level of Parkin expression via SIRT1. Blockade of SIRT1 inhibited the role of liraglutide on Parkin. By contrast, activation of SIRT1 was able to reverse the alteration in Parkin expression under hypoxic condition. *P

    Journal: Molecular Medicine Reports

    Article Title: Liraglutide repairs the infarcted heart: The role of the SIRT1/Parkin/mitophagy pathway

    doi: 10.3892/mmr.2018.8371

    Figure Lengend Snippet: Liraglutide activates Parkin via the SIRT1 pathway. (A) Western blotting and (B) densitometric analysis was used to detect the alterations in SIRT1 in the infarcted heart. Liraglutide was able to sustain the expression level of SIRT1 in a dose-dependent manner. In vitro , total proteins were isolated and analyzed via (C) western blotting to measure the alterations in (D) SIRT1 and (E) Parkin expression. SRT, the activator of SIRT1, was applied in the control group under hypoxia conditions. SRT elevated the expression levels of SIRT1 and Parkin in the context of hypoxic stimulation. Selisistat, the inhibitor of SIRT1, was used in the liraglutide-treated cells. Selisistat blocked the promotive effect of liraglutide on SIRT1 and Parkin expression. (F) Caspase9 activity and (G) LDH release assays were used to detect cell viability and mitochondrial apoptosis, respectively. (H) Co-staining of SIRT1 and Parkin. Liraglutide enhanced the level of Parkin expression via SIRT1. Blockade of SIRT1 inhibited the role of liraglutide on Parkin. By contrast, activation of SIRT1 was able to reverse the alteration in Parkin expression under hypoxic condition. *P

    Article Snippet: The primaries antibodies used in the present study were against the following proteins: Pro-caspase3 (1:1,000; Cell Signaling Technology, Inc.; cat. no. 9662), cleaved caspase3 (1:1,000; Cell Signaling Technology, Inc.; cat. no. 9664), baculoviral IAP repeat-containing protein 2 (c-IAP1; 1:2,000; Cell Signaling Technology, Inc. cat. no. 7065), caspase9 (1:1,000; Abcam; cat. no. ab32539), Parkin (1:1,000; Cell Signaling Technology, Inc.; cat. no. 2132), microtubule-associated protein light chain (LC) 3II (1:1,000; Cell Signaling Technology, Inc.; cat. no. 3868), sequestome-1 (p62; 1:1,000; Abcam; cat. no. ab56416), Beclin1 (1:1,000; Cell Signaling Technology, Inc.; cat. no. 3495), autophagy protein 5 (Atg5; 1:1,000; Cell Signaling Technology, Inc.; cat. no. 12,994), Sirt1 (1:1,000; Cell Signaling Technology, Inc., cat. no. 9475), TGFβ (1:1,000; Cell Signaling Technology, Inc.; cat. no. 3711), matrix metalloproteinase (MMP) 9 (1:1,000; Cell Signaling Technology, Inc.; cat. no. 13667) and poly (ADP ribose) polymerase 1 (PARP; 1:1,000; Cell Signaling Technology, Inc.; cat. no. 9532) The mean densities of the bands were represented as the optical density in units/mm2 and normalized to that of β -actin (Quantity One, version 4.6.2; Bio-Rad Laboratories, Inc.).

    Techniques: Western Blot, Expressing, In Vitro, Isolation, Activity Assay, Staining, Activation Assay

    Immunocytochemistry showed that caspase-3 was activated. The shrunken cells were positively stained for activated caspase-3. No positive cell was detectable in the control group ( A: original magnification, × 200). Whereas large numbers of positive cells labeled for activated caspase-3 were observed in HepG2 cells treated with 30 μmol/L troglitazone for 24 h ( B: original magnification, × 400).

    Journal: World Journal of Gastroenterology : WJG

    Article Title: Troglitazone, a peroxisome proliferator-activated receptor ? ligand, induces growth inhibition and apoptosis of HepG2 human liver cancer cells

    doi: 10.3748/wjg.14.2168

    Figure Lengend Snippet: Immunocytochemistry showed that caspase-3 was activated. The shrunken cells were positively stained for activated caspase-3. No positive cell was detectable in the control group ( A: original magnification, × 200). Whereas large numbers of positive cells labeled for activated caspase-3 were observed in HepG2 cells treated with 30 μmol/L troglitazone for 24 h ( B: original magnification, × 400).

    Article Snippet: After initiation of the apoptotic process, caspase-3 transforms from the zymogen form to the activated form and functions by hydrolyzing proteins essential for survival of many kinds of cells[ ].

    Techniques: Immunocytochemistry, Staining, Labeling

    Inhibitory effect of combined treatment with BAI and GEM on the proliferation of the human CFPAC-1 pancreatic cancer cell line in vivo . Representative images of (A) mice and (B) tumors. (C) Tumor volume changes in the xenografts. Resected tumors revealed that combination therapy decreased the tumor volume significantly compared with either the control group or the BAI-alone treated group. The data are presented as the mean ± SEM. (D) Following 28 days of treatment, the tumor weights were significantly decreased in all 3 treatment groups compared with the control group. The data are presented as the mean ± SEM. Representative immunohistochemical staining images and quantification for (E) Bcl-2, (F) Bax, (G) caspase-3 and (H) survivin from all groups of mice following treatment with BAI alone, GEM alone or a combination of the 2 treatments. Images were captured using a light microscope at a magnification of ×20. **P

    Journal: Oncology Letters

    Article Title: Inhibitory effect of baicalein combined with gemcitabine in human pancreatic cancer cell lines

    doi: 10.3892/ol.2018.8043

    Figure Lengend Snippet: Inhibitory effect of combined treatment with BAI and GEM on the proliferation of the human CFPAC-1 pancreatic cancer cell line in vivo . Representative images of (A) mice and (B) tumors. (C) Tumor volume changes in the xenografts. Resected tumors revealed that combination therapy decreased the tumor volume significantly compared with either the control group or the BAI-alone treated group. The data are presented as the mean ± SEM. (D) Following 28 days of treatment, the tumor weights were significantly decreased in all 3 treatment groups compared with the control group. The data are presented as the mean ± SEM. Representative immunohistochemical staining images and quantification for (E) Bcl-2, (F) Bax, (G) caspase-3 and (H) survivin from all groups of mice following treatment with BAI alone, GEM alone or a combination of the 2 treatments. Images were captured using a light microscope at a magnification of ×20. **P

    Article Snippet: Following deparaffinization, the sections were incubated at 4°C overnight with antibodies of Bcl-2 (cat no. 15071), Bax (cat no. 5023), caspase-3 (cat no. 9662) and survivin (cat no. 2808) (1:500; Cell Signaling Technology, Inc.).

    Techniques: In Vivo, Mouse Assay, Immunohistochemistry, Staining, Light Microscopy

    Effects of BAI alone, GEM alone or combined treatment on the protein expression levels of Bax, Bcl-2, caspase-3, PARP and survivin in the human CFPAC-1 pancreatic cancer cell line. (A) Representative images of Bax, Bcl-2, caspase-3, PARP and survivin protein expression, generated using a western blot analysis. β-actin was used as a loading control. Quantification of the intensity of (B) Bax, (C) Bcl-2, (D) caspase-3, (E) PARP and (F) and survivin. **P

    Journal: Oncology Letters

    Article Title: Inhibitory effect of baicalein combined with gemcitabine in human pancreatic cancer cell lines

    doi: 10.3892/ol.2018.8043

    Figure Lengend Snippet: Effects of BAI alone, GEM alone or combined treatment on the protein expression levels of Bax, Bcl-2, caspase-3, PARP and survivin in the human CFPAC-1 pancreatic cancer cell line. (A) Representative images of Bax, Bcl-2, caspase-3, PARP and survivin protein expression, generated using a western blot analysis. β-actin was used as a loading control. Quantification of the intensity of (B) Bax, (C) Bcl-2, (D) caspase-3, (E) PARP and (F) and survivin. **P

    Article Snippet: Following deparaffinization, the sections were incubated at 4°C overnight with antibodies of Bcl-2 (cat no. 15071), Bax (cat no. 5023), caspase-3 (cat no. 9662) and survivin (cat no. 2808) (1:500; Cell Signaling Technology, Inc.).

    Techniques: Expressing, Generated, Western Blot

    Tumor cell apoptosis is induced by AdC7-SP/E1A-ΔE3 via a p53-independent mitochondrial pathway NCI-H508 and Huh7 cells were infected at 100 MOI with AdC7-ΔE1-ΔE3, AdC7-ΔE3, and AdC7-SP/E1A-ΔE3. NCI-H508 cells were collected at 12 h and 24 h post infection, and Huh7 cells were collected 24 h and 48 h post-infection. Western blotting was carried out to detect levels of p53, phosphorylation of p53, MCL-1, Bcl-2, Bcl-xl, Bik and phosphorylation of Bad in NCI-H508 and Huh7 cells. β-actin was used as a loading control.

    Journal: Oncotarget

    Article Title: A novel oncolytic adenovirus based on simian adenovirus serotype 24

    doi: 10.18632/oncotarget.15845

    Figure Lengend Snippet: Tumor cell apoptosis is induced by AdC7-SP/E1A-ΔE3 via a p53-independent mitochondrial pathway NCI-H508 and Huh7 cells were infected at 100 MOI with AdC7-ΔE1-ΔE3, AdC7-ΔE3, and AdC7-SP/E1A-ΔE3. NCI-H508 cells were collected at 12 h and 24 h post infection, and Huh7 cells were collected 24 h and 48 h post-infection. Western blotting was carried out to detect levels of p53, phosphorylation of p53, MCL-1, Bcl-2, Bcl-xl, Bik and phosphorylation of Bad in NCI-H508 and Huh7 cells. β-actin was used as a loading control.

    Article Snippet: Protein expression levels were detected following transfer to PVDF membranes (Millipore, Bedford, MA); incubation with primary antibodies for Survivin, Cleaved Caspase-3, Cleaved PARP, p62, LC3A/B, p53, Phospho-p53 (Ser46), Mcl-1, Bcl-2, Bcl-xl, Bik or Phospho-Bad (Ser112) (Cell Signaling Technology, Danvers, MA); and subsequent incubation with secondary horseradish peroxidase-conjugated antibodies (Sigma-Aldrich, St Louis, MO).

    Techniques: Infection, Western Blot