phosphorylated p erk1 2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated p erk1 2
    Effects of benzidine on the expression and activation of mitogen-activated protein kinases and activating protein-1 monomers. (A) Total and <t>phosphorylated</t> <t>ERK1/2,</t> p38 and JNK protein levels were determined by western blotting. The levels of <t>p-ERK1/2,</t> p-p38 and p-JNK increased without any significant changes to total ERK1/2, p38 or JNK levels, indicating that benzidine exposure activated ERK1/2, p38, and JNK. The alterations to p-ERK1/2, p-p38 and p-JNK protein level occurred particularly at concentrations of 0.005 or 0.01 µM benzidine. (B) Densitometric quantification of the data from A. (C) Western blotting analysis of Jun family proteins. Significant increases in p-c-Jun and JunB levels were observed, whereas the JunD level was not significantly increased. (D) Densitometric quantification of the data from C. (E) The Fos family, including p-c-Fos, FosB and Fra-1, were all upregulated. (F) Densitometric quantification of the data from E. Densitometric data are expressed as the mean ± standard deviations of three independent experiments. p-, phosphorylated; ERK1/2, extracellular regulated protein kinases 1 and 2; JNK, Jun N-terminal kinase; Fra-1, Fos-like antigen 1.
    Phosphorylated P Erk1 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/phosphorylated p erk1 2/product/Cell Signaling Technology Inc
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    phosphorylated p erk1 2 - by Bioz Stars, 2023-03
    90/100 stars

    Images

    1) Product Images from "MAPK/AP-1 pathway regulates benzidine-induced cell proliferation through the control of cell cycle in human normal bladder epithelial cells"

    Article Title: MAPK/AP-1 pathway regulates benzidine-induced cell proliferation through the control of cell cycle in human normal bladder epithelial cells

    Journal: Oncology Letters

    doi: 10.3892/ol.2018.9155

    Effects of benzidine on the expression and activation of mitogen-activated protein kinases and activating protein-1 monomers. (A) Total and phosphorylated ERK1/2, p38 and JNK protein levels were determined by western blotting. The levels of p-ERK1/2, p-p38 and p-JNK increased without any significant changes to total ERK1/2, p38 or JNK levels, indicating that benzidine exposure activated ERK1/2, p38, and JNK. The alterations to p-ERK1/2, p-p38 and p-JNK protein level occurred particularly at concentrations of 0.005 or 0.01 µM benzidine. (B) Densitometric quantification of the data from A. (C) Western blotting analysis of Jun family proteins. Significant increases in p-c-Jun and JunB levels were observed, whereas the JunD level was not significantly increased. (D) Densitometric quantification of the data from C. (E) The Fos family, including p-c-Fos, FosB and Fra-1, were all upregulated. (F) Densitometric quantification of the data from E. Densitometric data are expressed as the mean ± standard deviations of three independent experiments. p-, phosphorylated; ERK1/2, extracellular regulated protein kinases 1 and 2; JNK, Jun N-terminal kinase; Fra-1, Fos-like antigen 1.
    Figure Legend Snippet: Effects of benzidine on the expression and activation of mitogen-activated protein kinases and activating protein-1 monomers. (A) Total and phosphorylated ERK1/2, p38 and JNK protein levels were determined by western blotting. The levels of p-ERK1/2, p-p38 and p-JNK increased without any significant changes to total ERK1/2, p38 or JNK levels, indicating that benzidine exposure activated ERK1/2, p38, and JNK. The alterations to p-ERK1/2, p-p38 and p-JNK protein level occurred particularly at concentrations of 0.005 or 0.01 µM benzidine. (B) Densitometric quantification of the data from A. (C) Western blotting analysis of Jun family proteins. Significant increases in p-c-Jun and JunB levels were observed, whereas the JunD level was not significantly increased. (D) Densitometric quantification of the data from C. (E) The Fos family, including p-c-Fos, FosB and Fra-1, were all upregulated. (F) Densitometric quantification of the data from E. Densitometric data are expressed as the mean ± standard deviations of three independent experiments. p-, phosphorylated; ERK1/2, extracellular regulated protein kinases 1 and 2; JNK, Jun N-terminal kinase; Fra-1, Fos-like antigen 1.

    Techniques Used: Expressing, Activation Assay, Western Blot

    Proliferation-inducing effect of benzidine on SV-HUC-1 cells was reversed by MAPK inhibitors. (A) The relative cell proliferation was suppressed by MAPK pathway inhibitors. The effect of the p38 inhibitor was the most distinct, as no increase in cell proliferation following the treatment with benzidine was observed. Western blot of SV-HUC-1 cells treated with benzidine and (B) U0126, an ERK1/2 inhibitor, (C) SB203580, a p38 inhibitor or (D) SP600125, a Jun N-terminal kinase inhibitor, for 6 days. Following the treatment with the MAPK inhibitors, the effect of benzidine treatment on cyclin D1 and p21 expression levels was suppressed; however, the increase in PCNA protein levels were inhibited only by U0126. Data is expressed as the means ± standard deviation of three independent experiments for each treatment. **P<0.01 vs. control; #P<0.05 vs. control+U0126. SV-HUC-1, SV-40 immortalized human uroepithelial cells; MAPK, mitogen-activated protein kinase; ERK1/2, extracellular regulated protein kinases 1 and 2; PCNA, proliferating cell nuclear antigen.
    Figure Legend Snippet: Proliferation-inducing effect of benzidine on SV-HUC-1 cells was reversed by MAPK inhibitors. (A) The relative cell proliferation was suppressed by MAPK pathway inhibitors. The effect of the p38 inhibitor was the most distinct, as no increase in cell proliferation following the treatment with benzidine was observed. Western blot of SV-HUC-1 cells treated with benzidine and (B) U0126, an ERK1/2 inhibitor, (C) SB203580, a p38 inhibitor or (D) SP600125, a Jun N-terminal kinase inhibitor, for 6 days. Following the treatment with the MAPK inhibitors, the effect of benzidine treatment on cyclin D1 and p21 expression levels was suppressed; however, the increase in PCNA protein levels were inhibited only by U0126. Data is expressed as the means ± standard deviation of three independent experiments for each treatment. **P<0.01 vs. control; #P<0.05 vs. control+U0126. SV-HUC-1, SV-40 immortalized human uroepithelial cells; MAPK, mitogen-activated protein kinase; ERK1/2, extracellular regulated protein kinases 1 and 2; PCNA, proliferating cell nuclear antigen.

    Techniques Used: Western Blot, Expressing, Standard Deviation

    phosphorylated p erk1 2  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc phosphorylated p erk1 2
    Effects of benzidine on the expression and activation of mitogen-activated protein kinases and activating protein-1 monomers. (A) Total and <t>phosphorylated</t> <t>ERK1/2,</t> p38 and JNK protein levels were determined by western blotting. The levels of <t>p-ERK1/2,</t> p-p38 and p-JNK increased without any significant changes to total ERK1/2, p38 or JNK levels, indicating that benzidine exposure activated ERK1/2, p38, and JNK. The alterations to p-ERK1/2, p-p38 and p-JNK protein level occurred particularly at concentrations of 0.005 or 0.01 µM benzidine. (B) Densitometric quantification of the data from A. (C) Western blotting analysis of Jun family proteins. Significant increases in p-c-Jun and JunB levels were observed, whereas the JunD level was not significantly increased. (D) Densitometric quantification of the data from C. (E) The Fos family, including p-c-Fos, FosB and Fra-1, were all upregulated. (F) Densitometric quantification of the data from E. Densitometric data are expressed as the mean ± standard deviations of three independent experiments. p-, phosphorylated; ERK1/2, extracellular regulated protein kinases 1 and 2; JNK, Jun N-terminal kinase; Fra-1, Fos-like antigen 1.
    Phosphorylated P Erk1 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/phosphorylated p erk1 2/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    phosphorylated p erk1 2 - by Bioz Stars, 2023-03
    86/100 stars

    Images

    1) Product Images from "MAPK/AP-1 pathway regulates benzidine-induced cell proliferation through the control of cell cycle in human normal bladder epithelial cells"

    Article Title: MAPK/AP-1 pathway regulates benzidine-induced cell proliferation through the control of cell cycle in human normal bladder epithelial cells

    Journal: Oncology Letters

    doi: 10.3892/ol.2018.9155

    Effects of benzidine on the expression and activation of mitogen-activated protein kinases and activating protein-1 monomers. (A) Total and phosphorylated ERK1/2, p38 and JNK protein levels were determined by western blotting. The levels of p-ERK1/2, p-p38 and p-JNK increased without any significant changes to total ERK1/2, p38 or JNK levels, indicating that benzidine exposure activated ERK1/2, p38, and JNK. The alterations to p-ERK1/2, p-p38 and p-JNK protein level occurred particularly at concentrations of 0.005 or 0.01 µM benzidine. (B) Densitometric quantification of the data from A. (C) Western blotting analysis of Jun family proteins. Significant increases in p-c-Jun and JunB levels were observed, whereas the JunD level was not significantly increased. (D) Densitometric quantification of the data from C. (E) The Fos family, including p-c-Fos, FosB and Fra-1, were all upregulated. (F) Densitometric quantification of the data from E. Densitometric data are expressed as the mean ± standard deviations of three independent experiments. p-, phosphorylated; ERK1/2, extracellular regulated protein kinases 1 and 2; JNK, Jun N-terminal kinase; Fra-1, Fos-like antigen 1.
    Figure Legend Snippet: Effects of benzidine on the expression and activation of mitogen-activated protein kinases and activating protein-1 monomers. (A) Total and phosphorylated ERK1/2, p38 and JNK protein levels were determined by western blotting. The levels of p-ERK1/2, p-p38 and p-JNK increased without any significant changes to total ERK1/2, p38 or JNK levels, indicating that benzidine exposure activated ERK1/2, p38, and JNK. The alterations to p-ERK1/2, p-p38 and p-JNK protein level occurred particularly at concentrations of 0.005 or 0.01 µM benzidine. (B) Densitometric quantification of the data from A. (C) Western blotting analysis of Jun family proteins. Significant increases in p-c-Jun and JunB levels were observed, whereas the JunD level was not significantly increased. (D) Densitometric quantification of the data from C. (E) The Fos family, including p-c-Fos, FosB and Fra-1, were all upregulated. (F) Densitometric quantification of the data from E. Densitometric data are expressed as the mean ± standard deviations of three independent experiments. p-, phosphorylated; ERK1/2, extracellular regulated protein kinases 1 and 2; JNK, Jun N-terminal kinase; Fra-1, Fos-like antigen 1.

    Techniques Used: Expressing, Activation Assay, Western Blot

    Proliferation-inducing effect of benzidine on SV-HUC-1 cells was reversed by MAPK inhibitors. (A) The relative cell proliferation was suppressed by MAPK pathway inhibitors. The effect of the p38 inhibitor was the most distinct, as no increase in cell proliferation following the treatment with benzidine was observed. Western blot of SV-HUC-1 cells treated with benzidine and (B) U0126, an ERK1/2 inhibitor, (C) SB203580, a p38 inhibitor or (D) SP600125, a Jun N-terminal kinase inhibitor, for 6 days. Following the treatment with the MAPK inhibitors, the effect of benzidine treatment on cyclin D1 and p21 expression levels was suppressed; however, the increase in PCNA protein levels were inhibited only by U0126. Data is expressed as the means ± standard deviation of three independent experiments for each treatment. **P<0.01 vs. control; #P<0.05 vs. control+U0126. SV-HUC-1, SV-40 immortalized human uroepithelial cells; MAPK, mitogen-activated protein kinase; ERK1/2, extracellular regulated protein kinases 1 and 2; PCNA, proliferating cell nuclear antigen.
    Figure Legend Snippet: Proliferation-inducing effect of benzidine on SV-HUC-1 cells was reversed by MAPK inhibitors. (A) The relative cell proliferation was suppressed by MAPK pathway inhibitors. The effect of the p38 inhibitor was the most distinct, as no increase in cell proliferation following the treatment with benzidine was observed. Western blot of SV-HUC-1 cells treated with benzidine and (B) U0126, an ERK1/2 inhibitor, (C) SB203580, a p38 inhibitor or (D) SP600125, a Jun N-terminal kinase inhibitor, for 6 days. Following the treatment with the MAPK inhibitors, the effect of benzidine treatment on cyclin D1 and p21 expression levels was suppressed; however, the increase in PCNA protein levels were inhibited only by U0126. Data is expressed as the means ± standard deviation of three independent experiments for each treatment. **P<0.01 vs. control; #P<0.05 vs. control+U0126. SV-HUC-1, SV-40 immortalized human uroepithelial cells; MAPK, mitogen-activated protein kinase; ERK1/2, extracellular regulated protein kinases 1 and 2; PCNA, proliferating cell nuclear antigen.

    Techniques Used: Western Blot, Expressing, Standard Deviation

    phosphorylated p erk1 2  (Cell Signaling Technology Inc)


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    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
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    Structured Review

    Cell Signaling Technology Inc phosphorylated p erk1 2
    Effects of benzidine on the expression and activation of mitogen-activated protein kinases and activating protein-1 monomers. (A) Total and <t>phosphorylated</t> <t>ERK1/2,</t> p38 and JNK protein levels were determined by western blotting. The levels of <t>p-ERK1/2,</t> p-p38 and p-JNK increased without any significant changes to total ERK1/2, p38 or JNK levels, indicating that benzidine exposure activated ERK1/2, p38, and JNK. The alterations to p-ERK1/2, p-p38 and p-JNK protein level occurred particularly at concentrations of 0.005 or 0.01 µM benzidine. (B) Densitometric quantification of the data from A. (C) Western blotting analysis of Jun family proteins. Significant increases in p-c-Jun and JunB levels were observed, whereas the JunD level was not significantly increased. (D) Densitometric quantification of the data from C. (E) The Fos family, including p-c-Fos, FosB and Fra-1, were all upregulated. (F) Densitometric quantification of the data from E. Densitometric data are expressed as the mean ± standard deviations of three independent experiments. p-, phosphorylated; ERK1/2, extracellular regulated protein kinases 1 and 2; JNK, Jun N-terminal kinase; Fra-1, Fos-like antigen 1.
    Phosphorylated P Erk1 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/phosphorylated p erk1 2/product/Cell Signaling Technology Inc
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    phosphorylated p erk1 2 - by Bioz Stars, 2023-03
    90/100 stars

    Images

    1) Product Images from "MAPK/AP-1 pathway regulates benzidine-induced cell proliferation through the control of cell cycle in human normal bladder epithelial cells"

    Article Title: MAPK/AP-1 pathway regulates benzidine-induced cell proliferation through the control of cell cycle in human normal bladder epithelial cells

    Journal: Oncology Letters

    doi: 10.3892/ol.2018.9155

    Effects of benzidine on the expression and activation of mitogen-activated protein kinases and activating protein-1 monomers. (A) Total and phosphorylated ERK1/2, p38 and JNK protein levels were determined by western blotting. The levels of p-ERK1/2, p-p38 and p-JNK increased without any significant changes to total ERK1/2, p38 or JNK levels, indicating that benzidine exposure activated ERK1/2, p38, and JNK. The alterations to p-ERK1/2, p-p38 and p-JNK protein level occurred particularly at concentrations of 0.005 or 0.01 µM benzidine. (B) Densitometric quantification of the data from A. (C) Western blotting analysis of Jun family proteins. Significant increases in p-c-Jun and JunB levels were observed, whereas the JunD level was not significantly increased. (D) Densitometric quantification of the data from C. (E) The Fos family, including p-c-Fos, FosB and Fra-1, were all upregulated. (F) Densitometric quantification of the data from E. Densitometric data are expressed as the mean ± standard deviations of three independent experiments. p-, phosphorylated; ERK1/2, extracellular regulated protein kinases 1 and 2; JNK, Jun N-terminal kinase; Fra-1, Fos-like antigen 1.
    Figure Legend Snippet: Effects of benzidine on the expression and activation of mitogen-activated protein kinases and activating protein-1 monomers. (A) Total and phosphorylated ERK1/2, p38 and JNK protein levels were determined by western blotting. The levels of p-ERK1/2, p-p38 and p-JNK increased without any significant changes to total ERK1/2, p38 or JNK levels, indicating that benzidine exposure activated ERK1/2, p38, and JNK. The alterations to p-ERK1/2, p-p38 and p-JNK protein level occurred particularly at concentrations of 0.005 or 0.01 µM benzidine. (B) Densitometric quantification of the data from A. (C) Western blotting analysis of Jun family proteins. Significant increases in p-c-Jun and JunB levels were observed, whereas the JunD level was not significantly increased. (D) Densitometric quantification of the data from C. (E) The Fos family, including p-c-Fos, FosB and Fra-1, were all upregulated. (F) Densitometric quantification of the data from E. Densitometric data are expressed as the mean ± standard deviations of three independent experiments. p-, phosphorylated; ERK1/2, extracellular regulated protein kinases 1 and 2; JNK, Jun N-terminal kinase; Fra-1, Fos-like antigen 1.

    Techniques Used: Expressing, Activation Assay, Western Blot

    Proliferation-inducing effect of benzidine on SV-HUC-1 cells was reversed by MAPK inhibitors. (A) The relative cell proliferation was suppressed by MAPK pathway inhibitors. The effect of the p38 inhibitor was the most distinct, as no increase in cell proliferation following the treatment with benzidine was observed. Western blot of SV-HUC-1 cells treated with benzidine and (B) U0126, an ERK1/2 inhibitor, (C) SB203580, a p38 inhibitor or (D) SP600125, a Jun N-terminal kinase inhibitor, for 6 days. Following the treatment with the MAPK inhibitors, the effect of benzidine treatment on cyclin D1 and p21 expression levels was suppressed; however, the increase in PCNA protein levels were inhibited only by U0126. Data is expressed as the means ± standard deviation of three independent experiments for each treatment. **P<0.01 vs. control; #P<0.05 vs. control+U0126. SV-HUC-1, SV-40 immortalized human uroepithelial cells; MAPK, mitogen-activated protein kinase; ERK1/2, extracellular regulated protein kinases 1 and 2; PCNA, proliferating cell nuclear antigen.
    Figure Legend Snippet: Proliferation-inducing effect of benzidine on SV-HUC-1 cells was reversed by MAPK inhibitors. (A) The relative cell proliferation was suppressed by MAPK pathway inhibitors. The effect of the p38 inhibitor was the most distinct, as no increase in cell proliferation following the treatment with benzidine was observed. Western blot of SV-HUC-1 cells treated with benzidine and (B) U0126, an ERK1/2 inhibitor, (C) SB203580, a p38 inhibitor or (D) SP600125, a Jun N-terminal kinase inhibitor, for 6 days. Following the treatment with the MAPK inhibitors, the effect of benzidine treatment on cyclin D1 and p21 expression levels was suppressed; however, the increase in PCNA protein levels were inhibited only by U0126. Data is expressed as the means ± standard deviation of three independent experiments for each treatment. **P<0.01 vs. control; #P<0.05 vs. control+U0126. SV-HUC-1, SV-40 immortalized human uroepithelial cells; MAPK, mitogen-activated protein kinase; ERK1/2, extracellular regulated protein kinases 1 and 2; PCNA, proliferating cell nuclear antigen.

    Techniques Used: Western Blot, Expressing, Standard Deviation

    phosphorylated p erk1 2  (Cell Signaling Technology Inc)


    Bioz Verified Symbol Cell Signaling Technology Inc is a verified supplier
    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
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    Structured Review

    Cell Signaling Technology Inc phosphorylated p erk1 2
    Effects of benzidine on the expression and activation of mitogen-activated protein kinases and activating protein-1 monomers. (A) Total and <t>phosphorylated</t> <t>ERK1/2,</t> p38 and JNK protein levels were determined by western blotting. The levels of <t>p-ERK1/2,</t> p-p38 and p-JNK increased without any significant changes to total ERK1/2, p38 or JNK levels, indicating that benzidine exposure activated ERK1/2, p38, and JNK. The alterations to p-ERK1/2, p-p38 and p-JNK protein level occurred particularly at concentrations of 0.005 or 0.01 µM benzidine. (B) Densitometric quantification of the data from A. (C) Western blotting analysis of Jun family proteins. Significant increases in p-c-Jun and JunB levels were observed, whereas the JunD level was not significantly increased. (D) Densitometric quantification of the data from C. (E) The Fos family, including p-c-Fos, FosB and Fra-1, were all upregulated. (F) Densitometric quantification of the data from E. Densitometric data are expressed as the mean ± standard deviations of three independent experiments. p-, phosphorylated; ERK1/2, extracellular regulated protein kinases 1 and 2; JNK, Jun N-terminal kinase; Fra-1, Fos-like antigen 1.
    Phosphorylated P Erk1 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/phosphorylated p erk1 2/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    phosphorylated p erk1 2 - by Bioz Stars, 2023-03
    86/100 stars

    Images

    1) Product Images from "MAPK/AP-1 pathway regulates benzidine-induced cell proliferation through the control of cell cycle in human normal bladder epithelial cells"

    Article Title: MAPK/AP-1 pathway regulates benzidine-induced cell proliferation through the control of cell cycle in human normal bladder epithelial cells

    Journal: Oncology Letters

    doi: 10.3892/ol.2018.9155

    Effects of benzidine on the expression and activation of mitogen-activated protein kinases and activating protein-1 monomers. (A) Total and phosphorylated ERK1/2, p38 and JNK protein levels were determined by western blotting. The levels of p-ERK1/2, p-p38 and p-JNK increased without any significant changes to total ERK1/2, p38 or JNK levels, indicating that benzidine exposure activated ERK1/2, p38, and JNK. The alterations to p-ERK1/2, p-p38 and p-JNK protein level occurred particularly at concentrations of 0.005 or 0.01 µM benzidine. (B) Densitometric quantification of the data from A. (C) Western blotting analysis of Jun family proteins. Significant increases in p-c-Jun and JunB levels were observed, whereas the JunD level was not significantly increased. (D) Densitometric quantification of the data from C. (E) The Fos family, including p-c-Fos, FosB and Fra-1, were all upregulated. (F) Densitometric quantification of the data from E. Densitometric data are expressed as the mean ± standard deviations of three independent experiments. p-, phosphorylated; ERK1/2, extracellular regulated protein kinases 1 and 2; JNK, Jun N-terminal kinase; Fra-1, Fos-like antigen 1.
    Figure Legend Snippet: Effects of benzidine on the expression and activation of mitogen-activated protein kinases and activating protein-1 monomers. (A) Total and phosphorylated ERK1/2, p38 and JNK protein levels were determined by western blotting. The levels of p-ERK1/2, p-p38 and p-JNK increased without any significant changes to total ERK1/2, p38 or JNK levels, indicating that benzidine exposure activated ERK1/2, p38, and JNK. The alterations to p-ERK1/2, p-p38 and p-JNK protein level occurred particularly at concentrations of 0.005 or 0.01 µM benzidine. (B) Densitometric quantification of the data from A. (C) Western blotting analysis of Jun family proteins. Significant increases in p-c-Jun and JunB levels were observed, whereas the JunD level was not significantly increased. (D) Densitometric quantification of the data from C. (E) The Fos family, including p-c-Fos, FosB and Fra-1, were all upregulated. (F) Densitometric quantification of the data from E. Densitometric data are expressed as the mean ± standard deviations of three independent experiments. p-, phosphorylated; ERK1/2, extracellular regulated protein kinases 1 and 2; JNK, Jun N-terminal kinase; Fra-1, Fos-like antigen 1.

    Techniques Used: Expressing, Activation Assay, Western Blot

    Proliferation-inducing effect of benzidine on SV-HUC-1 cells was reversed by MAPK inhibitors. (A) The relative cell proliferation was suppressed by MAPK pathway inhibitors. The effect of the p38 inhibitor was the most distinct, as no increase in cell proliferation following the treatment with benzidine was observed. Western blot of SV-HUC-1 cells treated with benzidine and (B) U0126, an ERK1/2 inhibitor, (C) SB203580, a p38 inhibitor or (D) SP600125, a Jun N-terminal kinase inhibitor, for 6 days. Following the treatment with the MAPK inhibitors, the effect of benzidine treatment on cyclin D1 and p21 expression levels was suppressed; however, the increase in PCNA protein levels were inhibited only by U0126. Data is expressed as the means ± standard deviation of three independent experiments for each treatment. **P<0.01 vs. control; #P<0.05 vs. control+U0126. SV-HUC-1, SV-40 immortalized human uroepithelial cells; MAPK, mitogen-activated protein kinase; ERK1/2, extracellular regulated protein kinases 1 and 2; PCNA, proliferating cell nuclear antigen.
    Figure Legend Snippet: Proliferation-inducing effect of benzidine on SV-HUC-1 cells was reversed by MAPK inhibitors. (A) The relative cell proliferation was suppressed by MAPK pathway inhibitors. The effect of the p38 inhibitor was the most distinct, as no increase in cell proliferation following the treatment with benzidine was observed. Western blot of SV-HUC-1 cells treated with benzidine and (B) U0126, an ERK1/2 inhibitor, (C) SB203580, a p38 inhibitor or (D) SP600125, a Jun N-terminal kinase inhibitor, for 6 days. Following the treatment with the MAPK inhibitors, the effect of benzidine treatment on cyclin D1 and p21 expression levels was suppressed; however, the increase in PCNA protein levels were inhibited only by U0126. Data is expressed as the means ± standard deviation of three independent experiments for each treatment. **P<0.01 vs. control; #P<0.05 vs. control+U0126. SV-HUC-1, SV-40 immortalized human uroepithelial cells; MAPK, mitogen-activated protein kinase; ERK1/2, extracellular regulated protein kinases 1 and 2; PCNA, proliferating cell nuclear antigen.

    Techniques Used: Western Blot, Expressing, Standard Deviation

    erk1 2  (Cell Signaling Technology Inc)


    Bioz Verified Symbol Cell Signaling Technology Inc is a verified supplier
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    Structured Review

    Cell Signaling Technology Inc erk1 2
    (A) Expression of proteins involved in the mitogen-activated protein kinase pathway, <t>including</t> <t>p-ERK1/2,</t> p-p38 and p-JNK, in SV-HUC-1 cells following treatment with 0.10, 0.25 and 0.50% CSE for 7 days. p-ERK1/2, p-P38 and p-JNK protein expression was increased following CSE treatment. (B) Expression of proteins involved in activator protein 1 pathway, including p-c-Jun, p-c-Fos, Jun B and Jun D in SV-HUC-1 cells following treatment with CSE for 7 days. The expression of p-c-Jun, p-c-Fos and Jun B were markedly increased following CSE treatment. p-, phosphorylated; ERK, extracellular signal regulated protein kinase; JNK, Jun N-terminal kinase; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.
    Erk1 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/erk1 2/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    erk1 2 - by Bioz Stars, 2023-03
    86/100 stars

    Images

    1) Product Images from "Cigarette smoke extract-induced proliferation of normal human urothelial cells via the MAPK/AP-1 pathway"

    Article Title: Cigarette smoke extract-induced proliferation of normal human urothelial cells via the MAPK/AP-1 pathway

    Journal: Oncology Letters

    doi: 10.3892/ol.2016.5407

    (A) Expression of proteins involved in the mitogen-activated protein kinase pathway, including p-ERK1/2, p-p38 and p-JNK, in SV-HUC-1 cells following treatment with 0.10, 0.25 and 0.50% CSE for 7 days. p-ERK1/2, p-P38 and p-JNK protein expression was increased following CSE treatment. (B) Expression of proteins involved in activator protein 1 pathway, including p-c-Jun, p-c-Fos, Jun B and Jun D in SV-HUC-1 cells following treatment with CSE for 7 days. The expression of p-c-Jun, p-c-Fos and Jun B were markedly increased following CSE treatment. p-, phosphorylated; ERK, extracellular signal regulated protein kinase; JNK, Jun N-terminal kinase; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.
    Figure Legend Snippet: (A) Expression of proteins involved in the mitogen-activated protein kinase pathway, including p-ERK1/2, p-p38 and p-JNK, in SV-HUC-1 cells following treatment with 0.10, 0.25 and 0.50% CSE for 7 days. p-ERK1/2, p-P38 and p-JNK protein expression was increased following CSE treatment. (B) Expression of proteins involved in activator protein 1 pathway, including p-c-Jun, p-c-Fos, Jun B and Jun D in SV-HUC-1 cells following treatment with CSE for 7 days. The expression of p-c-Jun, p-c-Fos and Jun B were markedly increased following CSE treatment. p-, phosphorylated; ERK, extracellular signal regulated protein kinase; JNK, Jun N-terminal kinase; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.

    Techniques Used: Expressing

    erk1 2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc erk1 2
    (A) Expression of proteins involved in the mitogen-activated protein kinase pathway, <t>including</t> <t>p-ERK1/2,</t> p-p38 and p-JNK, in SV-HUC-1 cells following treatment with 0.10, 0.25 and 0.50% CSE for 7 days. p-ERK1/2, p-P38 and p-JNK protein expression was increased following CSE treatment. (B) Expression of proteins involved in activator protein 1 pathway, including p-c-Jun, p-c-Fos, Jun B and Jun D in SV-HUC-1 cells following treatment with CSE for 7 days. The expression of p-c-Jun, p-c-Fos and Jun B were markedly increased following CSE treatment. p-, phosphorylated; ERK, extracellular signal regulated protein kinase; JNK, Jun N-terminal kinase; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.
    Erk1 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/erk1 2/product/Cell Signaling Technology Inc
    Average 90 stars, based on 1 article reviews
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    erk1 2 - by Bioz Stars, 2023-03
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    1) Product Images from "Cigarette smoke extract-induced proliferation of normal human urothelial cells via the MAPK/AP-1 pathway"

    Article Title: Cigarette smoke extract-induced proliferation of normal human urothelial cells via the MAPK/AP-1 pathway

    Journal: Oncology Letters

    doi: 10.3892/ol.2016.5407

    (A) Expression of proteins involved in the mitogen-activated protein kinase pathway, including p-ERK1/2, p-p38 and p-JNK, in SV-HUC-1 cells following treatment with 0.10, 0.25 and 0.50% CSE for 7 days. p-ERK1/2, p-P38 and p-JNK protein expression was increased following CSE treatment. (B) Expression of proteins involved in activator protein 1 pathway, including p-c-Jun, p-c-Fos, Jun B and Jun D in SV-HUC-1 cells following treatment with CSE for 7 days. The expression of p-c-Jun, p-c-Fos and Jun B were markedly increased following CSE treatment. p-, phosphorylated; ERK, extracellular signal regulated protein kinase; JNK, Jun N-terminal kinase; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.
    Figure Legend Snippet: (A) Expression of proteins involved in the mitogen-activated protein kinase pathway, including p-ERK1/2, p-p38 and p-JNK, in SV-HUC-1 cells following treatment with 0.10, 0.25 and 0.50% CSE for 7 days. p-ERK1/2, p-P38 and p-JNK protein expression was increased following CSE treatment. (B) Expression of proteins involved in activator protein 1 pathway, including p-c-Jun, p-c-Fos, Jun B and Jun D in SV-HUC-1 cells following treatment with CSE for 7 days. The expression of p-c-Jun, p-c-Fos and Jun B were markedly increased following CSE treatment. p-, phosphorylated; ERK, extracellular signal regulated protein kinase; JNK, Jun N-terminal kinase; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.

    Techniques Used: Expressing

    erk1 2  (Cell Signaling Technology Inc)


    Bioz Verified Symbol Cell Signaling Technology Inc is a verified supplier
    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
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    Cell Signaling Technology Inc erk1 2
    (A) Expression of proteins involved in the mitogen-activated protein kinase pathway, <t>including</t> <t>p-ERK1/2,</t> p-p38 and p-JNK, in SV-HUC-1 cells following treatment with 0.10, 0.25 and 0.50% CSE for 7 days. p-ERK1/2, p-P38 and p-JNK protein expression was increased following CSE treatment. (B) Expression of proteins involved in activator protein 1 pathway, including p-c-Jun, p-c-Fos, Jun B and Jun D in SV-HUC-1 cells following treatment with CSE for 7 days. The expression of p-c-Jun, p-c-Fos and Jun B were markedly increased following CSE treatment. p-, phosphorylated; ERK, extracellular signal regulated protein kinase; JNK, Jun N-terminal kinase; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.
    Erk1 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/erk1 2/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    erk1 2 - by Bioz Stars, 2023-03
    86/100 stars

    Images

    1) Product Images from "Cigarette smoke extract-induced proliferation of normal human urothelial cells via the MAPK/AP-1 pathway"

    Article Title: Cigarette smoke extract-induced proliferation of normal human urothelial cells via the MAPK/AP-1 pathway

    Journal: Oncology Letters

    doi: 10.3892/ol.2016.5407

    (A) Expression of proteins involved in the mitogen-activated protein kinase pathway, including p-ERK1/2, p-p38 and p-JNK, in SV-HUC-1 cells following treatment with 0.10, 0.25 and 0.50% CSE for 7 days. p-ERK1/2, p-P38 and p-JNK protein expression was increased following CSE treatment. (B) Expression of proteins involved in activator protein 1 pathway, including p-c-Jun, p-c-Fos, Jun B and Jun D in SV-HUC-1 cells following treatment with CSE for 7 days. The expression of p-c-Jun, p-c-Fos and Jun B were markedly increased following CSE treatment. p-, phosphorylated; ERK, extracellular signal regulated protein kinase; JNK, Jun N-terminal kinase; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.
    Figure Legend Snippet: (A) Expression of proteins involved in the mitogen-activated protein kinase pathway, including p-ERK1/2, p-p38 and p-JNK, in SV-HUC-1 cells following treatment with 0.10, 0.25 and 0.50% CSE for 7 days. p-ERK1/2, p-P38 and p-JNK protein expression was increased following CSE treatment. (B) Expression of proteins involved in activator protein 1 pathway, including p-c-Jun, p-c-Fos, Jun B and Jun D in SV-HUC-1 cells following treatment with CSE for 7 days. The expression of p-c-Jun, p-c-Fos and Jun B were markedly increased following CSE treatment. p-, phosphorylated; ERK, extracellular signal regulated protein kinase; JNK, Jun N-terminal kinase; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.

    Techniques Used: Expressing

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