Structured Review

Elabscience rabbit anti gapdh
Aβ 1–42 induces ER stress and up-regulated MANF expression in SH-SY5Y cells. a Representative images of MANF (red) and BiP (green) immunofluorescence labeling of SH-SY5Y cells incubated with DMEM containing 10% FBS, serum-free DMEM, and DMEM containing Aβ 1–42 (10 μM) for 24 h, or DMEM containing tunicamycin (TM) (2.5 μg/ml) for 12 h, respectively. The nuclei were stained with DAPI (blue). The enlarged images show the expression and cellular distribution of MANF and BiP, respectively. Scale bar = 10 μm. b Representative images of MANF (red) and CHOP (green) immunofluorescence labeling of SH-SY5Y cells incubated with 10% FBS, serum-free DMEM, and DMEM containing Aβ 1–42 (10 μM) for 24 h, or DMEM containing TM (2.5 μg/ml) for 12 h, respectively. The enlarged images show the expression and cellular distribution of MANF and CHOP, respectively. Scale bar = 10 μm. c Quantitation of MANF , BiP , and CHOP mRNA levels in SH-SY5Y cells treated with DMEM containing 10% FBS, serum-free DMEM, DMEM containing Aβ 1–42 (10 μM) for 24 h, or DMEM containing TM (2.5 μg/ml) for 12 h, respectively. <t>GAPDH</t> was used as control. d The protein levels of MANF, BiP, CHOP, and cleaved caspase-3 in SH-SY5Y cells treated as indicated. <t>α-tubulin</t> was used as a loading control. e Quantitation of protein levels normalized to the α-tubulin by densitometry in d. All the quantitative data were presented as mean ± SD of at least three independent experiments.* P
Rabbit Anti Gapdh, supplied by Elabscience, used in various techniques. Bioz Stars score: 93/100, based on 31 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 31 article reviews
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rabbit anti gapdh - by Bioz Stars, 2020-09
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Images

1) Product Images from "Mesencephalic astrocyte-derived neurotrophic factor (MANF) protects against Aβ toxicity via attenuating Aβ-induced endoplasmic reticulum stress"

Article Title: Mesencephalic astrocyte-derived neurotrophic factor (MANF) protects against Aβ toxicity via attenuating Aβ-induced endoplasmic reticulum stress

Journal: Journal of Neuroinflammation

doi: 10.1186/s12974-019-1429-0

Aβ 1–42 induces ER stress and up-regulated MANF expression in SH-SY5Y cells. a Representative images of MANF (red) and BiP (green) immunofluorescence labeling of SH-SY5Y cells incubated with DMEM containing 10% FBS, serum-free DMEM, and DMEM containing Aβ 1–42 (10 μM) for 24 h, or DMEM containing tunicamycin (TM) (2.5 μg/ml) for 12 h, respectively. The nuclei were stained with DAPI (blue). The enlarged images show the expression and cellular distribution of MANF and BiP, respectively. Scale bar = 10 μm. b Representative images of MANF (red) and CHOP (green) immunofluorescence labeling of SH-SY5Y cells incubated with 10% FBS, serum-free DMEM, and DMEM containing Aβ 1–42 (10 μM) for 24 h, or DMEM containing TM (2.5 μg/ml) for 12 h, respectively. The enlarged images show the expression and cellular distribution of MANF and CHOP, respectively. Scale bar = 10 μm. c Quantitation of MANF , BiP , and CHOP mRNA levels in SH-SY5Y cells treated with DMEM containing 10% FBS, serum-free DMEM, DMEM containing Aβ 1–42 (10 μM) for 24 h, or DMEM containing TM (2.5 μg/ml) for 12 h, respectively. GAPDH was used as control. d The protein levels of MANF, BiP, CHOP, and cleaved caspase-3 in SH-SY5Y cells treated as indicated. α-tubulin was used as a loading control. e Quantitation of protein levels normalized to the α-tubulin by densitometry in d. All the quantitative data were presented as mean ± SD of at least three independent experiments.* P
Figure Legend Snippet: Aβ 1–42 induces ER stress and up-regulated MANF expression in SH-SY5Y cells. a Representative images of MANF (red) and BiP (green) immunofluorescence labeling of SH-SY5Y cells incubated with DMEM containing 10% FBS, serum-free DMEM, and DMEM containing Aβ 1–42 (10 μM) for 24 h, or DMEM containing tunicamycin (TM) (2.5 μg/ml) for 12 h, respectively. The nuclei were stained with DAPI (blue). The enlarged images show the expression and cellular distribution of MANF and BiP, respectively. Scale bar = 10 μm. b Representative images of MANF (red) and CHOP (green) immunofluorescence labeling of SH-SY5Y cells incubated with 10% FBS, serum-free DMEM, and DMEM containing Aβ 1–42 (10 μM) for 24 h, or DMEM containing TM (2.5 μg/ml) for 12 h, respectively. The enlarged images show the expression and cellular distribution of MANF and CHOP, respectively. Scale bar = 10 μm. c Quantitation of MANF , BiP , and CHOP mRNA levels in SH-SY5Y cells treated with DMEM containing 10% FBS, serum-free DMEM, DMEM containing Aβ 1–42 (10 μM) for 24 h, or DMEM containing TM (2.5 μg/ml) for 12 h, respectively. GAPDH was used as control. d The protein levels of MANF, BiP, CHOP, and cleaved caspase-3 in SH-SY5Y cells treated as indicated. α-tubulin was used as a loading control. e Quantitation of protein levels normalized to the α-tubulin by densitometry in d. All the quantitative data were presented as mean ± SD of at least three independent experiments.* P

Techniques Used: Expressing, Immunofluorescence, Labeling, Incubation, Staining, Quantitation Assay

2) Product Images from "A new inhibitor of glucose-6-phosphate dehydrogenase blocks pentose phosphate pathway and suppresses malignant proliferation and metastasis in vivo"

Article Title: A new inhibitor of glucose-6-phosphate dehydrogenase blocks pentose phosphate pathway and suppresses malignant proliferation and metastasis in vivo

Journal: Cell Death & Disease

doi: 10.1038/s41419-018-0635-5

Polydatin Inhibits G6PD causing redox imbalance, which leads to ER stress and cell death. a Viability assay (MTT) of UMSCC103 treated with polydatin (20 µM) and 4μ8c (IRE inhibitor), GSK2606414 (PERK inhibitor) or with siRNA for either IRE1 or PERK, 24 or 48 h posttreatment, respectively. b IF with CellROX (for oxidative stress determination), 24 h posttreatment (In fig S5 : menadione is used as positive control; N -acetylcysteine (NAC) is used as ROS scavenger; quantitative assay). c IF with ER-Tracker on UMSCC103 treated with polydatin in combination with NAC, 24 h posttreatment. d G6PD enzymatic assay on UMSCC103 cell lysates (the same assay performed with purified enzyme is found in Fig. S2C). e NADP + /NADPH ratio on polydatin-treated cells. f Invasion assay of UMSCC103 after polydatin treatment. * p
Figure Legend Snippet: Polydatin Inhibits G6PD causing redox imbalance, which leads to ER stress and cell death. a Viability assay (MTT) of UMSCC103 treated with polydatin (20 µM) and 4μ8c (IRE inhibitor), GSK2606414 (PERK inhibitor) or with siRNA for either IRE1 or PERK, 24 or 48 h posttreatment, respectively. b IF with CellROX (for oxidative stress determination), 24 h posttreatment (In fig S5 : menadione is used as positive control; N -acetylcysteine (NAC) is used as ROS scavenger; quantitative assay). c IF with ER-Tracker on UMSCC103 treated with polydatin in combination with NAC, 24 h posttreatment. d G6PD enzymatic assay on UMSCC103 cell lysates (the same assay performed with purified enzyme is found in Fig. S2C). e NADP + /NADPH ratio on polydatin-treated cells. f Invasion assay of UMSCC103 after polydatin treatment. * p

Techniques Used: Viability Assay, MTT Assay, Positive Control, Enzymatic Assay, Purification, Invasion Assay

3) Product Images from "Role of the IL-33/ST2/p38 signaling pathway in the immune response of corneal epithelial cells to Aspergillus fumigatus infection"

Article Title: Role of the IL-33/ST2/p38 signaling pathway in the immune response of corneal epithelial cells to Aspergillus fumigatus infection

Journal: International Journal of Ophthalmology

doi: 10.18240/ijo.2019.04.04

IL-33/ST2 signaling upregulated A. fumigatus -induced inflammatory responses via p38 activation in HCECs HCECs were exposed to A. fumigatus hyphae (5×10 6 ) with or without prior incubation of recombinant human IL-33 (10 ng/mL), soluble ST2 protein (10 ng/mL), or the MAPK p38 inhibitor SB203580 for 1h. A: Western blots for human phospho-p38 protein and total p38 protein. B, D: Cytokine ( IL-6 and IL-1β ) mRNA levels of cells treated with A. fumigatus hyphae (5×10 6 ) for 4h determined by qRT-PCR. C, E: Cytokine (IL-6 and IL-1β) protein levels from the culture supernatants of cells treated with A. fumigatus hyphae for 48h determined by ELISA. a P
Figure Legend Snippet: IL-33/ST2 signaling upregulated A. fumigatus -induced inflammatory responses via p38 activation in HCECs HCECs were exposed to A. fumigatus hyphae (5×10 6 ) with or without prior incubation of recombinant human IL-33 (10 ng/mL), soluble ST2 protein (10 ng/mL), or the MAPK p38 inhibitor SB203580 for 1h. A: Western blots for human phospho-p38 protein and total p38 protein. B, D: Cytokine ( IL-6 and IL-1β ) mRNA levels of cells treated with A. fumigatus hyphae (5×10 6 ) for 4h determined by qRT-PCR. C, E: Cytokine (IL-6 and IL-1β) protein levels from the culture supernatants of cells treated with A. fumigatus hyphae for 48h determined by ELISA. a P

Techniques Used: Activation Assay, Incubation, Recombinant, Western Blot, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

4) Product Images from "Effect of Insulin-Regulated FOXC2 Expression in Adipocyte Differentiation and Insulin Resistance"

Article Title: Effect of Insulin-Regulated FOXC2 Expression in Adipocyte Differentiation and Insulin Resistance

Journal: Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy

doi: 10.2147/DMSO.S262950

Adipocyte differentiation and Oil Red O staining. The ( A ) group was cultured with normal differentiation. Compared to NC siRNA group ( D ), the oil red staining was intensified in cells transfected with FOXC2 siRNA ( E ), indicating that the adipose differentiation of the cells was significantly increased. Compared to NC plasmid ( B ), oil Red O staining was reduced in FOXC2 overexpression group ( C ), suggesting a decreased fat formation.
Figure Legend Snippet: Adipocyte differentiation and Oil Red O staining. The ( A ) group was cultured with normal differentiation. Compared to NC siRNA group ( D ), the oil red staining was intensified in cells transfected with FOXC2 siRNA ( E ), indicating that the adipose differentiation of the cells was significantly increased. Compared to NC plasmid ( B ), oil Red O staining was reduced in FOXC2 overexpression group ( C ), suggesting a decreased fat formation.

Techniques Used: Staining, Cell Culture, Transfection, Plasmid Preparation, Over Expression

Results of plasmid enzymatic digestion. PGL3 basic plasmid was successfully connected into the 512T and 512C pro. In the figure, the right-most band 5 is Marker, band 1 is the double enzyme digestion product of pgl3-basic-FOXC2-pro-512-T, band 2 is the double enzyme digestion product of pgl3-basic-FOXC2-pro-512-C, band 3 is the PGL3-FOXC2-pro, and band 4 is the PGL3- empty.
Figure Legend Snippet: Results of plasmid enzymatic digestion. PGL3 basic plasmid was successfully connected into the 512T and 512C pro. In the figure, the right-most band 5 is Marker, band 1 is the double enzyme digestion product of pgl3-basic-FOXC2-pro-512-T, band 2 is the double enzyme digestion product of pgl3-basic-FOXC2-pro-512-C, band 3 is the PGL3-FOXC2-pro, and band 4 is the PGL3- empty.

Techniques Used: Plasmid Preparation, Marker

Expression of FOXC2 protein in adipocytes transfected with FOXC2 overexpression plasmid or siRNA. ***P
Figure Legend Snippet: Expression of FOXC2 protein in adipocytes transfected with FOXC2 overexpression plasmid or siRNA. ***P

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

Effect of insulin on FOXC2 promoters. Insulin significantly increase the FOXC2-pro-512T promoter activity. **P
Figure Legend Snippet: Effect of insulin on FOXC2 promoters. Insulin significantly increase the FOXC2-pro-512T promoter activity. **P

Techniques Used: Activity Assay

Expression of IR-related genes under different FOXC2 expression condition, with or without insulin induction. ***P
Figure Legend Snippet: Expression of IR-related genes under different FOXC2 expression condition, with or without insulin induction. ***P

Techniques Used: Expressing

FOXC2 protein expression in adipose mesenchymal stem cells. In both normal medium (complete medium) and differentiation medium, FOXC2 protein expression in adipocytes increased after insulin treatment. In differentiation medium, FOXC2 expression was significantly increased in the presence of 4nM insulin. ***P
Figure Legend Snippet: FOXC2 protein expression in adipose mesenchymal stem cells. In both normal medium (complete medium) and differentiation medium, FOXC2 protein expression in adipocytes increased after insulin treatment. In differentiation medium, FOXC2 expression was significantly increased in the presence of 4nM insulin. ***P

Techniques Used: Expressing

The electrophoretogram of the expression of the genes. Control: no insulin. NC: control siRNA; SH: FOXC2 siRNA; P: control Plasmid; FP: FOXC2 Plasmid.
Figure Legend Snippet: The electrophoretogram of the expression of the genes. Control: no insulin. NC: control siRNA; SH: FOXC2 siRNA; P: control Plasmid; FP: FOXC2 Plasmid.

Techniques Used: Expressing, Plasmid Preparation

5) Product Images from "A new inhibitor of glucose-6-phosphate dehydrogenase blocks pentose phosphate pathway and suppresses malignant proliferation and metastasis in vivo"

Article Title: A new inhibitor of glucose-6-phosphate dehydrogenase blocks pentose phosphate pathway and suppresses malignant proliferation and metastasis in vivo

Journal: Cell Death & Disease

doi: 10.1038/s41419-018-0635-5

Polydatin Inhibits G6PD causing redox imbalance, which leads to ER stress and cell death. a Viability assay (MTT) of UMSCC103 treated with polydatin (20 µM) and 4μ8c (IRE inhibitor), GSK2606414 (PERK inhibitor) or with siRNA for either IRE1 or PERK, 24 or 48 h posttreatment, respectively. b : menadione is used as positive control; N -acetylcysteine (NAC) is used as ROS scavenger; quantitative assay). c IF with ER-Tracker on UMSCC103 treated with polydatin in combination with NAC, 24 h posttreatment. d G6PD enzymatic assay on UMSCC103 cell lysates (the same assay performed with purified enzyme is found in Fig. S2C). e NADP + /NADPH ratio on polydatin-treated cells. f Invasion assay of UMSCC103 after polydatin treatment. * p
Figure Legend Snippet: Polydatin Inhibits G6PD causing redox imbalance, which leads to ER stress and cell death. a Viability assay (MTT) of UMSCC103 treated with polydatin (20 µM) and 4μ8c (IRE inhibitor), GSK2606414 (PERK inhibitor) or with siRNA for either IRE1 or PERK, 24 or 48 h posttreatment, respectively. b : menadione is used as positive control; N -acetylcysteine (NAC) is used as ROS scavenger; quantitative assay). c IF with ER-Tracker on UMSCC103 treated with polydatin in combination with NAC, 24 h posttreatment. d G6PD enzymatic assay on UMSCC103 cell lysates (the same assay performed with purified enzyme is found in Fig. S2C). e NADP + /NADPH ratio on polydatin-treated cells. f Invasion assay of UMSCC103 after polydatin treatment. * p

Techniques Used: Viability Assay, MTT Assay, Positive Control, Enzymatic Assay, Purification, Invasion Assay

6) Product Images from "Effect of the Orally Active Growth Hormone Secretagogue MK-677 on Somatic Growth in Rats"

Article Title: Effect of the Orally Active Growth Hormone Secretagogue MK-677 on Somatic Growth in Rats

Journal: Yonsei Medical Journal

doi: 10.3349/ymj.2018.59.10.1174

Effect of MK-677 on mRNA and protein expression of growth hormone (GH), GH-releasing hormone (GHRH), GH secretagogue receptor (GHSR), somatostatin (SST), somatostatin receptor (SSTR)-2, and SSTR-5 in the hypothalamus or pituitary gland. (A) Pituitary GH mRNA level, (B) hypothalamic GHRH mRNA level, (C) hypothalamic and pituitary GHSR mRNA level, (D) hypothalamic SST mRNA level, (E) pituitary SSTR-2 mRNA level, (F) pituitary SSTR-5 mRNA level, and (G) protein levels of GHSR and SST in the hypothalamus and SSTR-2 and SSTR-5 in the pituitary gland. n=4/treatment. * p
Figure Legend Snippet: Effect of MK-677 on mRNA and protein expression of growth hormone (GH), GH-releasing hormone (GHRH), GH secretagogue receptor (GHSR), somatostatin (SST), somatostatin receptor (SSTR)-2, and SSTR-5 in the hypothalamus or pituitary gland. (A) Pituitary GH mRNA level, (B) hypothalamic GHRH mRNA level, (C) hypothalamic and pituitary GHSR mRNA level, (D) hypothalamic SST mRNA level, (E) pituitary SSTR-2 mRNA level, (F) pituitary SSTR-5 mRNA level, and (G) protein levels of GHSR and SST in the hypothalamus and SSTR-2 and SSTR-5 in the pituitary gland. n=4/treatment. * p

Techniques Used: Expressing

7) Product Images from "A new inhibitor of glucose-6-phosphate dehydrogenase blocks pentose phosphate pathway and suppresses malignant proliferation and metastasis in vivo"

Article Title: A new inhibitor of glucose-6-phosphate dehydrogenase blocks pentose phosphate pathway and suppresses malignant proliferation and metastasis in vivo

Journal: Cell Death & Disease

doi: 10.1038/s41419-018-0635-5

Polydatin Inhibits G6PD causing redox imbalance, which leads to ER stress and cell death. a Viability assay (MTT) of UMSCC103 treated with polydatin (20 µM) and 4μ8c (IRE inhibitor), GSK2606414 (PERK inhibitor) or with siRNA for either IRE1 or PERK, 24 or 48 h posttreatment, respectively. b : menadione is used as positive control; N -acetylcysteine (NAC) is used as ROS scavenger; quantitative assay). c IF with ER-Tracker on UMSCC103 treated with polydatin in combination with NAC, 24 h posttreatment. d G6PD enzymatic assay on UMSCC103 cell lysates (the same assay performed with purified enzyme is found in Fig. S2C). e NADP + /NADPH ratio on polydatin-treated cells. f Invasion assay of UMSCC103 after polydatin treatment. * p
Figure Legend Snippet: Polydatin Inhibits G6PD causing redox imbalance, which leads to ER stress and cell death. a Viability assay (MTT) of UMSCC103 treated with polydatin (20 µM) and 4μ8c (IRE inhibitor), GSK2606414 (PERK inhibitor) or with siRNA for either IRE1 or PERK, 24 or 48 h posttreatment, respectively. b : menadione is used as positive control; N -acetylcysteine (NAC) is used as ROS scavenger; quantitative assay). c IF with ER-Tracker on UMSCC103 treated with polydatin in combination with NAC, 24 h posttreatment. d G6PD enzymatic assay on UMSCC103 cell lysates (the same assay performed with purified enzyme is found in Fig. S2C). e NADP + /NADPH ratio on polydatin-treated cells. f Invasion assay of UMSCC103 after polydatin treatment. * p

Techniques Used: Viability Assay, MTT Assay, Positive Control, Enzymatic Assay, Purification, Invasion Assay

8) Product Images from "A new inhibitor of glucose-6-phosphate dehydrogenase blocks pentose phosphate pathway and suppresses malignant proliferation and metastasis in vivo"

Article Title: A new inhibitor of glucose-6-phosphate dehydrogenase blocks pentose phosphate pathway and suppresses malignant proliferation and metastasis in vivo

Journal: Cell Death & Disease

doi: 10.1038/s41419-018-0635-5

Polydatin Inhibits G6PD causing redox imbalance, which leads to ER stress and cell death. a Viability assay (MTT) of UMSCC103 treated with polydatin (20 µM) and 4μ8c (IRE inhibitor), GSK2606414 (PERK inhibitor) or with siRNA for either IRE1 or PERK, 24 or 48 h posttreatment, respectively. b IF with CellROX (for oxidative stress determination), 24 h posttreatment (In fig S5 : menadione is used as positive control; N -acetylcysteine (NAC) is used as ROS scavenger; quantitative assay). c IF with ER-Tracker on UMSCC103 treated with polydatin in combination with NAC, 24 h posttreatment. d G6PD enzymatic assay on UMSCC103 cell lysates (the same assay performed with purified enzyme is found in Fig. S2C). e NADP + /NADPH ratio on polydatin-treated cells. f Invasion assay of UMSCC103 after polydatin treatment. * p
Figure Legend Snippet: Polydatin Inhibits G6PD causing redox imbalance, which leads to ER stress and cell death. a Viability assay (MTT) of UMSCC103 treated with polydatin (20 µM) and 4μ8c (IRE inhibitor), GSK2606414 (PERK inhibitor) or with siRNA for either IRE1 or PERK, 24 or 48 h posttreatment, respectively. b IF with CellROX (for oxidative stress determination), 24 h posttreatment (In fig S5 : menadione is used as positive control; N -acetylcysteine (NAC) is used as ROS scavenger; quantitative assay). c IF with ER-Tracker on UMSCC103 treated with polydatin in combination with NAC, 24 h posttreatment. d G6PD enzymatic assay on UMSCC103 cell lysates (the same assay performed with purified enzyme is found in Fig. S2C). e NADP + /NADPH ratio on polydatin-treated cells. f Invasion assay of UMSCC103 after polydatin treatment. * p

Techniques Used: Viability Assay, MTT Assay, Positive Control, Enzymatic Assay, Purification, Invasion Assay

9) Product Images from "Effect of the Orally Active Growth Hormone Secretagogue MK-677 on Somatic Growth in Rats"

Article Title: Effect of the Orally Active Growth Hormone Secretagogue MK-677 on Somatic Growth in Rats

Journal: Yonsei Medical Journal

doi: 10.3349/ymj.2018.59.10.1174

Effect of MK-677 on mRNA and protein expression of growth hormone (GH), GH-releasing hormone (GHRH), GH secretagogue receptor (GHSR), somatostatin (SST), somatostatin receptor (SSTR)-2, and SSTR-5 in the hypothalamus or pituitary gland. (A) Pituitary GH mRNA level, (B) hypothalamic GHRH mRNA level, (C) hypothalamic and pituitary GHSR mRNA level, (D) hypothalamic SST mRNA level, (E) pituitary SSTR-2 mRNA level, (F) pituitary SSTR-5 mRNA level, and (G) protein levels of GHSR and SST in the hypothalamus and SSTR-2 and SSTR-5 in the pituitary gland. n=4/treatment. * p
Figure Legend Snippet: Effect of MK-677 on mRNA and protein expression of growth hormone (GH), GH-releasing hormone (GHRH), GH secretagogue receptor (GHSR), somatostatin (SST), somatostatin receptor (SSTR)-2, and SSTR-5 in the hypothalamus or pituitary gland. (A) Pituitary GH mRNA level, (B) hypothalamic GHRH mRNA level, (C) hypothalamic and pituitary GHSR mRNA level, (D) hypothalamic SST mRNA level, (E) pituitary SSTR-2 mRNA level, (F) pituitary SSTR-5 mRNA level, and (G) protein levels of GHSR and SST in the hypothalamus and SSTR-2 and SSTR-5 in the pituitary gland. n=4/treatment. * p

Techniques Used: Expressing

10) Product Images from "Isoforsythiaside Attenuates Alzheimer’s Disease via Regulating Mitochondrial Function Through the PI3K/AKT Pathway"

Article Title: Isoforsythiaside Attenuates Alzheimer’s Disease via Regulating Mitochondrial Function Through the PI3K/AKT Pathway

Journal: International Journal of Molecular Sciences

doi: 10.3390/ijms21165687

IFY regulated the expression levels of mitochondrial apoptosis-related proteins. IFY ameliorated the expression levels of apoptosis related proteins including BAD, BAX, BCL-2, BCL-XL, BID, AIF, p-PI3K and p-AKT in ( A ) the hippocampus of APP/PS1 mice and ( B ) Aβ 1-42 -exposed U251 cells. Quantification data were normalized by glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and the corresponding total proteins, and are reported as the percentage of those from the corresponding CTRL ( n = 3). Data are shown as the mean ± SEM. # p
Figure Legend Snippet: IFY regulated the expression levels of mitochondrial apoptosis-related proteins. IFY ameliorated the expression levels of apoptosis related proteins including BAD, BAX, BCL-2, BCL-XL, BID, AIF, p-PI3K and p-AKT in ( A ) the hippocampus of APP/PS1 mice and ( B ) Aβ 1-42 -exposed U251 cells. Quantification data were normalized by glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and the corresponding total proteins, and are reported as the percentage of those from the corresponding CTRL ( n = 3). Data are shown as the mean ± SEM. # p

Techniques Used: Expressing, Mouse Assay

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Article Snippet: .. Filters were incubated overnight with the following antibodies: vinculin (1:600, MA5-11690, Invitrogen); PTX3 (C-10 1:600, sc-373951, Santa Cruz Biotechnology); phospho-p38 (Thr180) (1:500, E-AB-20949, Elabscience); p38 (1:500, E-AB-32460, Elabscience); ERK1/2 (1:500, E-AB-31374, Elabscience); phospho-ERK1/2 (Thr202) (1:500, E-AB-20868, Elabscience); PSMB5 (1:500, ab3330, Abcam); PSMB8 (1:500, Proteasome 20S LMP7, ab3329, Abcam); PSMB9 [1:500, Proteasome 20S LMP2 (EPR13785) ab184172, Abcam]; RAGE (1:500, NBP2-03950, Novusbio); S-100β chain (C-3) (1:500, sc-393919, Santa Cruz Biotechnology); monocyte chemoattractant protein (MCP)-1 (ECE.2) (1:500, sc-52701, Santa Cruz Biotechnology); Foxp3 (FJK-16s) (1:500, 14-5773-82, eBioscience); IL-33 (1:500, AF3626, R & D Systems); collagen VI (1:500, ab6588, Abcam); phospho-SMAD2/3 (Thr8) (1:500, E-AB-21040, Elabscience); TLR9 (26C593) (1:500, sc-52966, Santa Cruz Biotechnology); matrix metalloproteinase (MMP)-9 (E-11) (1:500, sc-393859, Santa Cruz Biotechnology); TLR4 (25) (1:500, sc-293072, Santa Cruz Biotechnology); TRAF6 (D-10) (1:500, sc-8409, Santa Cruz Biotechnology); SMAD3 (1:500, E-AB-32921, Elabscience); TLR2 (1:500, orb229137, Biorbyt); TLR5 (19D759.2) (1:500, sc-57461, Santa Cruz Biotechnology); NF-κB p65 (A-12) (1:500, sc-514451, Santa Cruz Biotechnology); RelB (D-4) (1:500, sc-48366, Santa Cruz Biotechnology); MYD88 (1:500, 23230-1-AP, Proteintech); transforming growth factor (TGF)β1 (1:500, E-AB-33090, Elabscience); IL-6 (10E5) (1:500, sc-57315, Santa Cruz Biotechnology); tumor necrosis factor (TNF)α (1:500, E-AB-40015, Elabscience); poly(ADP-ribose) polymerase (PPAR)γ (1:600, ab-59256, Abcam); autophagy-related (ATG)7 (1:600, SAB4200304, Sigma Aldrich); p62 (1:600, P0067, Sigma Aldrich); LC3B (1:500, L7543, Sigma Aldrich); HMGB1 (HAP46.5) (1:600, sc-56698, Santa Cruz Biotechnology); actin (1:600, A2066, Sigma Aldrich); GAPDH (0411) (1:600, sc-47724, Santa Cruz Biotechnology). .. Membranes were incubated with primary antibodies ON at 4°C, followed by washing, detection with horseradish peroxidase (HRP)-conjugated secondary antibodies (DakoCytomation, United States), and developed by enhanced chemiluminescence (ECL) (Amersham Biosciences, United States).

Article Title: Role of the IL-33/ST2/p38 signaling pathway in the immune response of corneal epithelial cells to Aspergillus fumigatus infection
Article Snippet: .. The membrane was then incubated with rabbit anti-IL-33(Santa Cruz Biotechnology, Santa Cruz, CA, USA) diluted 1:1000 followed by 1:5000 diluted goat anti-rabbit secondary antibody (Elabscience, Wuhan, China), or incubated with 1:1000 diluted rabbit anti-human poly-clonal antibodies against human phospho-p38 protein and total p38 (Elabscience), followed by incubation with 1:5000 diluted goat anti-rabbit IgG (Elabscience). .. The membrane was also blotted with a monoclonal anti-GAPDH antibody (Elabscience) as a loading control.

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    Anti Gapdh Ab, supplied by Elabscience, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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