sb 202190  (Millipore)

 
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  • 86
    Name:
    SB 202190
    Description:

    Catalog Number:
    S7067
    Price:
    None
    Applications:
    SB 202190 was used to inhibit p38 activation in MCF7 cells5, mouse macrophages6 and HepG2 cells.7
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    Structured Review

    Millipore sb 202190
    SB 202190

    https://www.bioz.com/result/sb 202190/product/Millipore
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    sb 202190 - by Bioz Stars, 2021-05
    86/100 stars

    Images

    1) Product Images from "CTRP9 Mediates Protective Effects in Cardiomyocytes via AMPK- and Adiponectin Receptor-Mediated Induction of Anti-Oxidant Response"

    Article Title: CTRP9 Mediates Protective Effects in Cardiomyocytes via AMPK- and Adiponectin Receptor-Mediated Induction of Anti-Oxidant Response

    Journal: Cells

    doi: 10.3390/cells9051229

    Signaling pathways involved in CTRP9 effects in cardiomyocytes and cardiomyoblasts. ( A ) Densitometry and representative Western blots, showing the time-dependent influence of CTRP9 (4 µg/mL) on the activation of AMPK, p44/42 MAPK, p38 MAPK and Akt in ARVCs. n = cells from 13–14 different animals per group. ( B ) Influence of AMPK inhibition with Ara A (500 µmol/L), p44/42 MAPK inhibition with U0126 (10 µmol/L) or p38 MAPK inhibition with SB 202190 (5 µmol/L) on CTRP9-mediated anti-oxidative effects as deduced from changes of DCFH-DA fluorescence in ARVCs in response to phenylephrine (10 µmol/L). Inhibitors were applied 30 min before CTRP9 (4 µg/mL, 24 h). n = cells from five different animals per group. ( C ): Mitochondrial and cytosolic ROS release in H9C2 cardiomyoblasts after alpha1 or alpha2-AMPK knockdown by siRNA. Mock transfected cells served as controls. 24 h after transfection, cells were pre-incubated with CTRP9 (4 µg/mL) for 24 h and then treated with phenylephrine. Knockdown efficiency (protein) is shown. Data from 5 independent experiments. ( D ) Influence of exclusive knockdown of AdipoR1, AdipoR2, or T-cadherin on CTRP9-mediated anti-oxidative effects as deduced from changes of DCFH-DA fluorescence in H9C2 cardiomyoblasts. Twenty-four hours after transfection, cells were pre-incubated with CTRP9 (4 µg/mL) for 24 h and then treated with phenylephrine. Knockdown efficiency (mRNA) is shown. Data from five independent experiments. ( E ) Influence of combined knockdown of AdipoR1 and AdipoR2 on CTRP9-mediated anti-oxidative effects as described in D. Data from five independent experiments. ( F ) Influence of knockdown of calreticulin or gC1qR on CTRP9-mediated anti-oxidative effects as described in D. Knockdown efficiency (protein) is shown. Data from five independent experiments. All data are mean ± SEM, * p
    Figure Legend Snippet: Signaling pathways involved in CTRP9 effects in cardiomyocytes and cardiomyoblasts. ( A ) Densitometry and representative Western blots, showing the time-dependent influence of CTRP9 (4 µg/mL) on the activation of AMPK, p44/42 MAPK, p38 MAPK and Akt in ARVCs. n = cells from 13–14 different animals per group. ( B ) Influence of AMPK inhibition with Ara A (500 µmol/L), p44/42 MAPK inhibition with U0126 (10 µmol/L) or p38 MAPK inhibition with SB 202190 (5 µmol/L) on CTRP9-mediated anti-oxidative effects as deduced from changes of DCFH-DA fluorescence in ARVCs in response to phenylephrine (10 µmol/L). Inhibitors were applied 30 min before CTRP9 (4 µg/mL, 24 h). n = cells from five different animals per group. ( C ): Mitochondrial and cytosolic ROS release in H9C2 cardiomyoblasts after alpha1 or alpha2-AMPK knockdown by siRNA. Mock transfected cells served as controls. 24 h after transfection, cells were pre-incubated with CTRP9 (4 µg/mL) for 24 h and then treated with phenylephrine. Knockdown efficiency (protein) is shown. Data from 5 independent experiments. ( D ) Influence of exclusive knockdown of AdipoR1, AdipoR2, or T-cadherin on CTRP9-mediated anti-oxidative effects as deduced from changes of DCFH-DA fluorescence in H9C2 cardiomyoblasts. Twenty-four hours after transfection, cells were pre-incubated with CTRP9 (4 µg/mL) for 24 h and then treated with phenylephrine. Knockdown efficiency (mRNA) is shown. Data from five independent experiments. ( E ) Influence of combined knockdown of AdipoR1 and AdipoR2 on CTRP9-mediated anti-oxidative effects as described in D. Data from five independent experiments. ( F ) Influence of knockdown of calreticulin or gC1qR on CTRP9-mediated anti-oxidative effects as described in D. Knockdown efficiency (protein) is shown. Data from five independent experiments. All data are mean ± SEM, * p

    Techniques Used: Western Blot, Activation Assay, Inhibition, Acetylene Reduction Assay, Fluorescence, Transfection, Incubation

    Related Articles

    Expressing:

    Article Title: MEKK1 plays a critical role in activating the transcription factor C/EBP-?-dependent gene expression in response to IFN-?
    Article Snippet: Because the p38 kinase is controlled by MEKK1, these results were expected. .. As observed in c- Raf +/+ and c- Raf −/− cells, SB202190, but not U0126 inhibited reporter gene expression in MEKK1 +/+ cells. .. Together these results indicate that MEKK1 is critical for IFN-γ-dependent gene expression.

    Concentration Assay:

    Article Title: The Plant-Derived Glucocorticoid Receptor Agonist Endiandrin A Acts as Co-Stimulator of Colonic Epithelial Sodium Channels (ENaC) via SGK-1 and MAPKs
    Article Snippet: TNF-α (TEBU, Offenbach, Germany) was used in a concentration of 500 IU/ml or 10,000 IU/ml in PBS. .. Specific inhibitors of MAPK, the p38 MAPK inhibitor SB202190, the p42/44 extracellular signal-regulated kinase (ERK, ERK’s upstream kinase MEK1/2) inhibitor U0126 and the JNK MAPK inhibitor SP600125 (Sigma-Aldrich) were used in a concentration of 10 µM. .. For GR antagonization RU-486 (10 µM; Sigma-Aldrich) was used.

    other:

    Article Title: Analysis of the transcriptional activity of endogenous NFAT5 in primary cells using transgenic NFAT-luciferase reporter mice
    Article Snippet: Reagents Phorbol 12-myristate 13-acetate (PMA), the calcium ionophore ionomycin, FK506, and the protein kinase inhibitors H89, LY294002, PD98059, SB202190, SB203580, SP600125 and wortmannin were purchased from Calbiochem (Darmstadt, Germany).

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    Millipore sb202190
    The effect of pharmacological inhibition of p38 MAPK on WA-mediated apoptosis in MCF-7 cells. The MCF-7 cells were pretreated with 10 μM <t>SB202190</t> for 1 h, exposed to 2.5 μM WA in the absence or presence of SB202190 for 24 h, and then processed for western blot analysis or apoptosis detection. (A) Western blotting for phosphorylated p38 MAPK and cleaved PARP. Quantitation for phosphorylated p38MAPK relative to DMSO-treated cells is shown. (B) Histone-associated DNA fragment release into the cytosol. Quantitation relative to DMSO-treated cells is shown. Combined results (n = 6) from two independent experiments are shown as mean ± S.D. Statistical significance was determined by one-way ANOVA with Bonferroni’s multiple comparison test. a Significantly different ( P
    Sb202190, 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
    https://www.bioz.com/result/sb202190/product/Millipore
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    sb202190 - by Bioz Stars, 2021-05
    99/100 stars
      Buy from Supplier

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    The effect of pharmacological inhibition of p38 MAPK on WA-mediated apoptosis in MCF-7 cells. The MCF-7 cells were pretreated with 10 μM SB202190 for 1 h, exposed to 2.5 μM WA in the absence or presence of SB202190 for 24 h, and then processed for western blot analysis or apoptosis detection. (A) Western blotting for phosphorylated p38 MAPK and cleaved PARP. Quantitation for phosphorylated p38MAPK relative to DMSO-treated cells is shown. (B) Histone-associated DNA fragment release into the cytosol. Quantitation relative to DMSO-treated cells is shown. Combined results (n = 6) from two independent experiments are shown as mean ± S.D. Statistical significance was determined by one-way ANOVA with Bonferroni’s multiple comparison test. a Significantly different ( P

    Journal: Molecular carcinogenesis

    Article Title: Role of Mitogen-Activated Protein Kinases and Mcl-1 in Apoptosis Induction by Withaferin A in Human Breast Cancer Cells

    doi: 10.1002/mc.22050

    Figure Lengend Snippet: The effect of pharmacological inhibition of p38 MAPK on WA-mediated apoptosis in MCF-7 cells. The MCF-7 cells were pretreated with 10 μM SB202190 for 1 h, exposed to 2.5 μM WA in the absence or presence of SB202190 for 24 h, and then processed for western blot analysis or apoptosis detection. (A) Western blotting for phosphorylated p38 MAPK and cleaved PARP. Quantitation for phosphorylated p38MAPK relative to DMSO-treated cells is shown. (B) Histone-associated DNA fragment release into the cytosol. Quantitation relative to DMSO-treated cells is shown. Combined results (n = 6) from two independent experiments are shown as mean ± S.D. Statistical significance was determined by one-way ANOVA with Bonferroni’s multiple comparison test. a Significantly different ( P

    Article Snippet: Pharmacological inhibitors of MAPK, including SB202190 (p38 MAPK inhibitor), SP600125 (JNK inhibitor), and PD98059 (inhibitor of an upstream kinase in ERK signaling pathway) were purchased from EMD-Millipore (Billerica, MA).

    Techniques: Inhibition, Western Blot, Quantitation Assay

    Synergistic ENaC induction by endiandrin A is linked to an activation of p38 and ERK in HT-29/B6-GR cells. HT-29/B6-GR cells were pre-incubated with the indicated MAPK inhibitors (10 µmol/L) for 1 hour before addition of dexamethasone (1 µM) and/or TNF-α (500 U/ml) and/or endiandrin A (20 µM) for 24 hours. ( A ) Measurement of ENaC-dependent Na + absorption as the drop in I SC after amiloride (100 µM) and measurement of γ-ENaC-mRNA after 24 hours. GAPDH was used for normalization of mRNA expression. Data are given as means ± s.e.m., n = 8–11 and n = 5–8, *** P

    Journal: PLoS ONE

    Article Title: The Plant-Derived Glucocorticoid Receptor Agonist Endiandrin A Acts as Co-Stimulator of Colonic Epithelial Sodium Channels (ENaC) via SGK-1 and MAPKs

    doi: 10.1371/journal.pone.0049426

    Figure Lengend Snippet: Synergistic ENaC induction by endiandrin A is linked to an activation of p38 and ERK in HT-29/B6-GR cells. HT-29/B6-GR cells were pre-incubated with the indicated MAPK inhibitors (10 µmol/L) for 1 hour before addition of dexamethasone (1 µM) and/or TNF-α (500 U/ml) and/or endiandrin A (20 µM) for 24 hours. ( A ) Measurement of ENaC-dependent Na + absorption as the drop in I SC after amiloride (100 µM) and measurement of γ-ENaC-mRNA after 24 hours. GAPDH was used for normalization of mRNA expression. Data are given as means ± s.e.m., n = 8–11 and n = 5–8, *** P

    Article Snippet: Specific inhibitors of MAPK, the p38 MAPK inhibitor SB202190, the p42/44 extracellular signal-regulated kinase (ERK, ERK’s upstream kinase MEK1/2) inhibitor U0126 and the JNK MAPK inhibitor SP600125 (Sigma-Aldrich) were used in a concentration of 10 µM.

    Techniques: Activation Assay, Incubation, Expressing

    Increasing doses of the p38 MAPK cascade inhibitor, SB202190, and the p42/44 MEK inhibitor, PD98059, inhibited eosinophil chemotaxis. Eosinophils (1 × 10 6 cells) were added with IL-5 (30 ng/ml) to the upper chambers of a transwell plate. Chemotaxis

    Journal: Journal of Innate Immunity

    Article Title: Eosinophils Utilize Multiple Chemokine Receptors for Chemotaxis to the Parasitic Nematode Strongyloides stercoralis

    doi: 10.1159/000233235

    Figure Lengend Snippet: Increasing doses of the p38 MAPK cascade inhibitor, SB202190, and the p42/44 MEK inhibitor, PD98059, inhibited eosinophil chemotaxis. Eosinophils (1 × 10 6 cells) were added with IL-5 (30 ng/ml) to the upper chambers of a transwell plate. Chemotaxis

    Article Snippet: Bordetella PTX and SB202190, a p38 inhibitor, were purchased from Calbiochem Inc. (San Diego, Calif., USA) Wortmannin, a PI3K inhibitor, and herbimycin A, a tyrosine kinase inhibitor, were purchased from Sigma Chemical Co.

    Techniques: Chemotaxis Assay

    Role of MAPK and NF-κB in the mannan induced SBD-1 expression in OREC. A OREC were treated with mannan and harvested at 0, 5, 15, 30, 45, and 60 min. Whole-cell lysates were prepared and used for Western blotting analysis with p38 and p-p38, ERK1/2 and p-ERK1/2, JNK and p-JNK, IκB and p-IκB, p65 and p-p65 antibodies. Protein levels are represented by the value shown in gray for the p-factor/factor. Statistical analyses were performed using the ImageJ software. B Effect of inhibitors on the mannan-induced SBD-1 mRNA expression was determined by qPCR. OREC were cultured with mannan, with or without the SB202190 p38 inhibitor, PD98059 ERK1/2 inhibitor, SP600125 JNK inhibitor, and PDTC NF-κB inhibitor. The relative mRNA abundance was calculated using the 2 −ΔΔCt method relative to β-actin. Data are mean ± SD ( n = 3). Different letters indicate significantly different means ( P

    Journal: Veterinary Research

    Article Title: Saccharomyces cerevisiae mannan induces sheep beta-defensin-1 expression via Dectin-2-Syk-p38 pathways in ovine ruminal epithelial cells

    doi: 10.1186/s13567-019-0624-4

    Figure Lengend Snippet: Role of MAPK and NF-κB in the mannan induced SBD-1 expression in OREC. A OREC were treated with mannan and harvested at 0, 5, 15, 30, 45, and 60 min. Whole-cell lysates were prepared and used for Western blotting analysis with p38 and p-p38, ERK1/2 and p-ERK1/2, JNK and p-JNK, IκB and p-IκB, p65 and p-p65 antibodies. Protein levels are represented by the value shown in gray for the p-factor/factor. Statistical analyses were performed using the ImageJ software. B Effect of inhibitors on the mannan-induced SBD-1 mRNA expression was determined by qPCR. OREC were cultured with mannan, with or without the SB202190 p38 inhibitor, PD98059 ERK1/2 inhibitor, SP600125 JNK inhibitor, and PDTC NF-κB inhibitor. The relative mRNA abundance was calculated using the 2 −ΔΔCt method relative to β-actin. Data are mean ± SD ( n = 3). Different letters indicate significantly different means ( P

    Article Snippet: Then, the downstream pathways were inhibited using specific inhibitors: SB202190 (20 μM, Sigma) for p38, PD98059 (20 μM, Sigma) for ERK1/2, SP600125 (20 μM, Sigma) for JNK, and PDTC (10 μM, Sigma) for NF-κB.

    Techniques: Expressing, Western Blot, Software, Real-time Polymerase Chain Reaction, Cell Culture