p38 mapk thr180 tyr182 Search Results


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  • 98
    Cell Signaling Technology Inc rabbit anti phospho p38 mapk
    The <t>MAPK</t> <t>and</t> <t>p38/MAPK</t> pathways couple light to MSK1 activation. Cannulated animals were infused with 3 μl of DMSO (vehicle), U0126, SB203508, or a combination of U0126 and SB203508 45 min before light exposure (15 min, 100 lux) at CT 22. A, Representative coronal tissue sections immunolabeled for phosphorylated MSK1. Boxed regions are magnified below each image. B, Average number of pMSK1-positive cells per SCN. Disruption of the MAPK pathway significantly reduced the number of positive cells relative to DMSO infusion. SB203508 attenuated light-induced MSK1 activation; however, this effect failed to reach significance relative to DMSO infused, light-treated animals (p > 0.06). The combined administration of U0126 and SB203508 blocked MSK1 phosphorylation. *p < 0.001, relative to the DMSO-infused light-treated condition. Numbers below each bar represent the number of animals used for each condition.
    Rabbit Anti Phospho P38 Mapk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti phospho p38 mapk/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti phospho p38 mapk - by Bioz Stars, 2023-02
    98/100 stars
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    99
    Cell Signaling Technology Inc antiphospho p38 mitogen activated protein kinase mapk
    The <t>MAPK</t> <t>and</t> <t>p38/MAPK</t> pathways couple light to MSK1 activation. Cannulated animals were infused with 3 μl of DMSO (vehicle), U0126, SB203508, or a combination of U0126 and SB203508 45 min before light exposure (15 min, 100 lux) at CT 22. A, Representative coronal tissue sections immunolabeled for phosphorylated MSK1. Boxed regions are magnified below each image. B, Average number of pMSK1-positive cells per SCN. Disruption of the MAPK pathway significantly reduced the number of positive cells relative to DMSO infusion. SB203508 attenuated light-induced MSK1 activation; however, this effect failed to reach significance relative to DMSO infused, light-treated animals (p > 0.06). The combined administration of U0126 and SB203508 blocked MSK1 phosphorylation. *p < 0.001, relative to the DMSO-infused light-treated condition. Numbers below each bar represent the number of animals used for each condition.
    Antiphospho P38 Mitogen Activated Protein Kinase Mapk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antiphospho p38 mitogen activated protein kinase mapk/product/Cell Signaling Technology Inc
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    antiphospho p38 mitogen activated protein kinase mapk - by Bioz Stars, 2023-02
    99/100 stars
      Buy from Supplier

    99
    Cell Signaling Technology Inc p p38
    The <t>MAPK</t> <t>and</t> <t>p38/MAPK</t> pathways couple light to MSK1 activation. Cannulated animals were infused with 3 μl of DMSO (vehicle), U0126, SB203508, or a combination of U0126 and SB203508 45 min before light exposure (15 min, 100 lux) at CT 22. A, Representative coronal tissue sections immunolabeled for phosphorylated MSK1. Boxed regions are magnified below each image. B, Average number of pMSK1-positive cells per SCN. Disruption of the MAPK pathway significantly reduced the number of positive cells relative to DMSO infusion. SB203508 attenuated light-induced MSK1 activation; however, this effect failed to reach significance relative to DMSO infused, light-treated animals (p > 0.06). The combined administration of U0126 and SB203508 blocked MSK1 phosphorylation. *p < 0.001, relative to the DMSO-infused light-treated condition. Numbers below each bar represent the number of animals used for each condition.
    P P38, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p p38/product/Cell Signaling Technology Inc
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p p38 - by Bioz Stars, 2023-02
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    97
    Cell Signaling Technology Inc p p38 mapk
    Effects of TA on constitutive and TGF-β2-stimulated signaling activities in cultured human RPE cells. (A) Human R-50 cells were treated with TA at 10 µM under serum-supplemented or -starved conditions for the indicated periods. Total proteins were subjected to western blot analysis of p-Smad2, p-ERK1/2 and <t>p-p38</t> <t>MAPK.</t> (B) Densitometric analysis of (A). (C) R-50 RPE cells received 2 h of serum starvation, followed by treatment with 10 ng/ml TGF-β2 in the presence or absence of 10 µM TA. (D) Densitometric analysis of (C). Data are presented as the mean ± SD from three independent experiments. # P<0.05 vs. respective 0 h group; *P<0.05 vs. respective TA (−) group. RPE, retinal pigment epithelial; TA, triamcinolone acetonide; TGF-β2, transforming growth factor-β2; p, phosphorylated; ERK1/2, extracellular-regulated kinase 1/2; MAPK, mitogen-activated protein kinase.
    P P38 Mapk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p p38 mapk/product/Cell Signaling Technology Inc
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p p38 mapk - by Bioz Stars, 2023-02
    97/100 stars
      Buy from Supplier

    99
    Cell Signaling Technology Inc anti phospho p38 mapk
    Effects of TA on constitutive and TGF-β2-stimulated signaling activities in cultured human RPE cells. (A) Human R-50 cells were treated with TA at 10 µM under serum-supplemented or -starved conditions for the indicated periods. Total proteins were subjected to western blot analysis of p-Smad2, p-ERK1/2 and <t>p-p38</t> <t>MAPK.</t> (B) Densitometric analysis of (A). (C) R-50 RPE cells received 2 h of serum starvation, followed by treatment with 10 ng/ml TGF-β2 in the presence or absence of 10 µM TA. (D) Densitometric analysis of (C). Data are presented as the mean ± SD from three independent experiments. # P<0.05 vs. respective 0 h group; *P<0.05 vs. respective TA (−) group. RPE, retinal pigment epithelial; TA, triamcinolone acetonide; TGF-β2, transforming growth factor-β2; p, phosphorylated; ERK1/2, extracellular-regulated kinase 1/2; MAPK, mitogen-activated protein kinase.
    Anti Phospho P38 Mapk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti phospho p38 mapk/product/Cell Signaling Technology Inc
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti phospho p38 mapk - by Bioz Stars, 2023-02
    99/100 stars
      Buy from Supplier

    Image Search Results


    The MAPK and p38/MAPK pathways couple light to MSK1 activation. Cannulated animals were infused with 3 μl of DMSO (vehicle), U0126, SB203508, or a combination of U0126 and SB203508 45 min before light exposure (15 min, 100 lux) at CT 22. A, Representative coronal tissue sections immunolabeled for phosphorylated MSK1. Boxed regions are magnified below each image. B, Average number of pMSK1-positive cells per SCN. Disruption of the MAPK pathway significantly reduced the number of positive cells relative to DMSO infusion. SB203508 attenuated light-induced MSK1 activation; however, this effect failed to reach significance relative to DMSO infused, light-treated animals (p > 0.06). The combined administration of U0126 and SB203508 blocked MSK1 phosphorylation. *p < 0.001, relative to the DMSO-infused light-treated condition. Numbers below each bar represent the number of animals used for each condition.

    Journal: The Journal of Neuroscience

    Article Title: Light Stimulates MSK1 Activation in the Suprachiasmatic Nucleus via a PACAP-ERK/MAP Kinase-Dependent Mechanism

    doi: 10.1523/JNEUROSCI.4361-04.2005

    Figure Lengend Snippet: The MAPK and p38/MAPK pathways couple light to MSK1 activation. Cannulated animals were infused with 3 μl of DMSO (vehicle), U0126, SB203508, or a combination of U0126 and SB203508 45 min before light exposure (15 min, 100 lux) at CT 22. A, Representative coronal tissue sections immunolabeled for phosphorylated MSK1. Boxed regions are magnified below each image. B, Average number of pMSK1-positive cells per SCN. Disruption of the MAPK pathway significantly reduced the number of positive cells relative to DMSO infusion. SB203508 attenuated light-induced MSK1 activation; however, this effect failed to reach significance relative to DMSO infused, light-treated animals (p > 0.06). The combined administration of U0126 and SB203508 blocked MSK1 phosphorylation. *p < 0.001, relative to the DMSO-infused light-treated condition. Numbers below each bar represent the number of animals used for each condition.

    Article Snippet: Tissue was then blocked (1 h) in 5% goat serum/PBST and incubated (overnight, 4°C) in rabbit anti-phospho-MSK1 (1:500 final dilution; Cell Signaling Technology, Beverly, MA), rabbit anti-phospho-ERK (1:2000; Cell Signaling Technology), or rabbit anti-phospho-p38/MAPK (1:1000; Cell Signaling Technology).

    Techniques: Activation Assay, Immunolabeling

    Effects of TA on constitutive and TGF-β2-stimulated signaling activities in cultured human RPE cells. (A) Human R-50 cells were treated with TA at 10 µM under serum-supplemented or -starved conditions for the indicated periods. Total proteins were subjected to western blot analysis of p-Smad2, p-ERK1/2 and p-p38 MAPK. (B) Densitometric analysis of (A). (C) R-50 RPE cells received 2 h of serum starvation, followed by treatment with 10 ng/ml TGF-β2 in the presence or absence of 10 µM TA. (D) Densitometric analysis of (C). Data are presented as the mean ± SD from three independent experiments. # P<0.05 vs. respective 0 h group; *P<0.05 vs. respective TA (−) group. RPE, retinal pigment epithelial; TA, triamcinolone acetonide; TGF-β2, transforming growth factor-β2; p, phosphorylated; ERK1/2, extracellular-regulated kinase 1/2; MAPK, mitogen-activated protein kinase.

    Journal: Molecular Medicine Reports

    Article Title: Triamcinolone acetonide modulates TGF-β2-induced angiogenic and tissue-remodeling effects in cultured human retinal pigment epithelial cells

    doi: 10.3892/mmr.2021.12442

    Figure Lengend Snippet: Effects of TA on constitutive and TGF-β2-stimulated signaling activities in cultured human RPE cells. (A) Human R-50 cells were treated with TA at 10 µM under serum-supplemented or -starved conditions for the indicated periods. Total proteins were subjected to western blot analysis of p-Smad2, p-ERK1/2 and p-p38 MAPK. (B) Densitometric analysis of (A). (C) R-50 RPE cells received 2 h of serum starvation, followed by treatment with 10 ng/ml TGF-β2 in the presence or absence of 10 µM TA. (D) Densitometric analysis of (C). Data are presented as the mean ± SD from three independent experiments. # P<0.05 vs. respective 0 h group; *P<0.05 vs. respective TA (−) group. RPE, retinal pigment epithelial; TA, triamcinolone acetonide; TGF-β2, transforming growth factor-β2; p, phosphorylated; ERK1/2, extracellular-regulated kinase 1/2; MAPK, mitogen-activated protein kinase.

    Article Snippet: Rabbit monoclonal antibodies against total Smad2 (cat. no. 5339s), phosphorylated (p)-Smad2 (Ser465/467; cat. no. 3108s), total ERK1/2 (cat. no. 4695s), p-ERK1/2 (Thr202/185 and Tyr204/187; cat. no. 9101s), total p38 MAPK (cat. no. 8690s) and p-p38 MAPK (Thr180/Tyr182; cat. no. 4631) were purchased from Cell Signaling Technology, Inc.

    Techniques: Cell Culture, Western Blot

    Suppressive effect of TA on TGF-β2-induced de novo synthesis of VEGF in cultured human retinal pigment epithelial cells. (A) Human R-50 cells were treated with TGF-β2 for 6 h in the presence of TA at the indicated doses or 0.1% MeOH as a SC. Total RNA was extracted and a multiplex reverse transcription-PCR was performed to simultaneously detect three isoforms of VEGF transcripts. (A) Representative gel showing VEGF isoform PCR products. (B) Densitometric analysis of the two major VEGF 121 and VEGF 165 transcripts. The density values of genes were normalized to those of the respective internal control, β-actin. Data are presented as the mean ± SD. (C) Reverse transcription-quantitative PCR analysis of the mRNA expression levels of VEGF 165 . TGF-β receptor blocker SB4 at 10 µM was used to block receptor kinase activity. (D) ELISA of R-50 cells receiving 10 ng/ml TGF-β2 for 48 h in the presence of 1 µM (TA1) or 10 µM (TA10) TA. (E) ELISA of R-50 cells receiving 10 ng/ml TGF-β2 for 24 h in the presence of p38 mitogen-activated protein kinase inhibitor SB2, MEK inhibitor PD, TGF-β receptor blocker SB4 at 10 µM or equivalent DMSO as a SC. Data are presented as the mean ± SD from three independent experiments. # P<0.05, ## P<0.01 vs. NC; *P<0.05, **P<0.01, ***P<0.001 vs. MeOH or vs. DMSO SC. TA, triamcinolone acetonide; TGF-β2, transforming growth factor-β2; VEGF, vascular endothelial growth factor; NC, negative control; SC, solvent control; SB4, SB431542; SB2, SB203580; PD, PD98059.

    Journal: Molecular Medicine Reports

    Article Title: Triamcinolone acetonide modulates TGF-β2-induced angiogenic and tissue-remodeling effects in cultured human retinal pigment epithelial cells

    doi: 10.3892/mmr.2021.12442

    Figure Lengend Snippet: Suppressive effect of TA on TGF-β2-induced de novo synthesis of VEGF in cultured human retinal pigment epithelial cells. (A) Human R-50 cells were treated with TGF-β2 for 6 h in the presence of TA at the indicated doses or 0.1% MeOH as a SC. Total RNA was extracted and a multiplex reverse transcription-PCR was performed to simultaneously detect three isoforms of VEGF transcripts. (A) Representative gel showing VEGF isoform PCR products. (B) Densitometric analysis of the two major VEGF 121 and VEGF 165 transcripts. The density values of genes were normalized to those of the respective internal control, β-actin. Data are presented as the mean ± SD. (C) Reverse transcription-quantitative PCR analysis of the mRNA expression levels of VEGF 165 . TGF-β receptor blocker SB4 at 10 µM was used to block receptor kinase activity. (D) ELISA of R-50 cells receiving 10 ng/ml TGF-β2 for 48 h in the presence of 1 µM (TA1) or 10 µM (TA10) TA. (E) ELISA of R-50 cells receiving 10 ng/ml TGF-β2 for 24 h in the presence of p38 mitogen-activated protein kinase inhibitor SB2, MEK inhibitor PD, TGF-β receptor blocker SB4 at 10 µM or equivalent DMSO as a SC. Data are presented as the mean ± SD from three independent experiments. # P<0.05, ## P<0.01 vs. NC; *P<0.05, **P<0.01, ***P<0.001 vs. MeOH or vs. DMSO SC. TA, triamcinolone acetonide; TGF-β2, transforming growth factor-β2; VEGF, vascular endothelial growth factor; NC, negative control; SC, solvent control; SB4, SB431542; SB2, SB203580; PD, PD98059.

    Article Snippet: Rabbit monoclonal antibodies against total Smad2 (cat. no. 5339s), phosphorylated (p)-Smad2 (Ser465/467; cat. no. 3108s), total ERK1/2 (cat. no. 4695s), p-ERK1/2 (Thr202/185 and Tyr204/187; cat. no. 9101s), total p38 MAPK (cat. no. 8690s) and p-p38 MAPK (Thr180/Tyr182; cat. no. 4631) were purchased from Cell Signaling Technology, Inc.

    Techniques: Cell Culture, Multiplex Assay, Real-time Polymerase Chain Reaction, Expressing, Blocking Assay, Activity Assay, Enzyme-linked Immunosorbent Assay, Negative Control

    Effect of TA treatment on TGF-β2-driven ECM remodeling in cultured human retinal pigment epithelial cells. (A) Western blot analysis of signaling pathway proteins involved in TGF-β2-driven ECM remodeling. Human R-50 cells were treated with 10 ng/ml TGF-β2 for 24 h in the presence of either 10 µM p38 mitogen-activated protein kinase inhibitor SB2, MEK inhibitor PD or equivalent DMSO as a SC. Bands were densitometrically semi-quantified and the relative expression levels of (B) COL1A1, (C) α-SMA, (D) MMP-9 and (E) MMP-2 were normalized to internal actin expression levels. (F) R-50 cells were treated with 10 ng/ml TGF-β2 for 48 h in the presence of 10 µM TA, TGF-β receptor blocker SB4 or 0.1% methanol as a SC. The relative expression levels of (G) COL1A1, (H) α-SMA, (I) MMP-9 and (J) MMP-2 were densitometrically semi-quantified and normalized to β-actin. Fold changes are expressed as the mean ± SD from three independent experiments. # P<0.05, ## P<0.01 vs. NC; *P<0.05, **P<0.01 vs. SC. TA, triamcinolone acetonide; TGF-β2, transforming growth factor-β2; α-SMA, α-smooth muscle actin; MMP, matrix metalloproteinase; NC, negative control; SC, solvent control; SB4, SB431542; SB2, SB203580; PD, PD98059; COL1A1, collagen type I α1 chain.

    Journal: Molecular Medicine Reports

    Article Title: Triamcinolone acetonide modulates TGF-β2-induced angiogenic and tissue-remodeling effects in cultured human retinal pigment epithelial cells

    doi: 10.3892/mmr.2021.12442

    Figure Lengend Snippet: Effect of TA treatment on TGF-β2-driven ECM remodeling in cultured human retinal pigment epithelial cells. (A) Western blot analysis of signaling pathway proteins involved in TGF-β2-driven ECM remodeling. Human R-50 cells were treated with 10 ng/ml TGF-β2 for 24 h in the presence of either 10 µM p38 mitogen-activated protein kinase inhibitor SB2, MEK inhibitor PD or equivalent DMSO as a SC. Bands were densitometrically semi-quantified and the relative expression levels of (B) COL1A1, (C) α-SMA, (D) MMP-9 and (E) MMP-2 were normalized to internal actin expression levels. (F) R-50 cells were treated with 10 ng/ml TGF-β2 for 48 h in the presence of 10 µM TA, TGF-β receptor blocker SB4 or 0.1% methanol as a SC. The relative expression levels of (G) COL1A1, (H) α-SMA, (I) MMP-9 and (J) MMP-2 were densitometrically semi-quantified and normalized to β-actin. Fold changes are expressed as the mean ± SD from three independent experiments. # P<0.05, ## P<0.01 vs. NC; *P<0.05, **P<0.01 vs. SC. TA, triamcinolone acetonide; TGF-β2, transforming growth factor-β2; α-SMA, α-smooth muscle actin; MMP, matrix metalloproteinase; NC, negative control; SC, solvent control; SB4, SB431542; SB2, SB203580; PD, PD98059; COL1A1, collagen type I α1 chain.

    Article Snippet: Rabbit monoclonal antibodies against total Smad2 (cat. no. 5339s), phosphorylated (p)-Smad2 (Ser465/467; cat. no. 3108s), total ERK1/2 (cat. no. 4695s), p-ERK1/2 (Thr202/185 and Tyr204/187; cat. no. 9101s), total p38 MAPK (cat. no. 8690s) and p-p38 MAPK (Thr180/Tyr182; cat. no. 4631) were purchased from Cell Signaling Technology, Inc.

    Techniques: Cell Culture, Western Blot, Expressing, Negative Control

    Effect of TA treatment on TGF-β2-driven MMP-9 gelatinolytic activity in cultured human retinal pigment epithelial cells. (A) Human R-50 cells were treated with TGF-β2 for 48 h in the presence of 1 µM (TA1) or 10 µM (TA10) TA or 0.1% MeOH as a SC. The supernatants were collected and subjected to gelatin zymography detection of MMP-9 activity. Bands were densitometrically semi-quantified and the scanned densities were subtracted from the background levels in the M group. (B) R50 cells were treated with TGF-β2 for 24 h in the presence of either 10 µM p38 mitogen-activated protein kinase inhibitor SB, MEK inhibitor PD or equivalent DMSO as a SC. Fold changes presented as the mean ± SD were obtained from three independent experiments. # P<0.05 vs. NC; *P<0.05 vs. MeOH or SC. TA, triamcinolone acetonide; TGF-β2, transforming growth factor-β2; MMP, matrix metalloproteinase; NC, negative control; SC, solvent control; M, medium; MeOH, methanol; SB, SB203580; PD, PD98059.

    Journal: Molecular Medicine Reports

    Article Title: Triamcinolone acetonide modulates TGF-β2-induced angiogenic and tissue-remodeling effects in cultured human retinal pigment epithelial cells

    doi: 10.3892/mmr.2021.12442

    Figure Lengend Snippet: Effect of TA treatment on TGF-β2-driven MMP-9 gelatinolytic activity in cultured human retinal pigment epithelial cells. (A) Human R-50 cells were treated with TGF-β2 for 48 h in the presence of 1 µM (TA1) or 10 µM (TA10) TA or 0.1% MeOH as a SC. The supernatants were collected and subjected to gelatin zymography detection of MMP-9 activity. Bands were densitometrically semi-quantified and the scanned densities were subtracted from the background levels in the M group. (B) R50 cells were treated with TGF-β2 for 24 h in the presence of either 10 µM p38 mitogen-activated protein kinase inhibitor SB, MEK inhibitor PD or equivalent DMSO as a SC. Fold changes presented as the mean ± SD were obtained from three independent experiments. # P<0.05 vs. NC; *P<0.05 vs. MeOH or SC. TA, triamcinolone acetonide; TGF-β2, transforming growth factor-β2; MMP, matrix metalloproteinase; NC, negative control; SC, solvent control; M, medium; MeOH, methanol; SB, SB203580; PD, PD98059.

    Article Snippet: Rabbit monoclonal antibodies against total Smad2 (cat. no. 5339s), phosphorylated (p)-Smad2 (Ser465/467; cat. no. 3108s), total ERK1/2 (cat. no. 4695s), p-ERK1/2 (Thr202/185 and Tyr204/187; cat. no. 9101s), total p38 MAPK (cat. no. 8690s) and p-p38 MAPK (Thr180/Tyr182; cat. no. 4631) were purchased from Cell Signaling Technology, Inc.

    Techniques: Activity Assay, Cell Culture, Zymography, Negative Control