p38 stress activated protein kinase sapk inhibitor sb202190  (Millipore)


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    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 p38 stress activated protein kinase sapk inhibitor sb202190
    SB 202190

    https://www.bioz.com/result/p38 stress activated protein kinase sapk inhibitor sb202190/product/Millipore
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p38 stress activated protein kinase sapk inhibitor sb202190 - by Bioz Stars, 2020-09
    99/100 stars

    Images

    1) Product Images from "Evidence for a Lack of a Direct Transcriptional Suppression of the Iron Regulatory Peptide Hepcidin by Hypoxia-Inducible Factors"

    Article Title: Evidence for a Lack of a Direct Transcriptional Suppression of the Iron Regulatory Peptide Hepcidin by Hypoxia-Inducible Factors

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0007875

    Response of hepcidin transcript levels to serum deprivation and protein kinase inhibition. ( A ) Serum withdrawal rapidly decreased hepcidin transcript levels in Huh7 cells. ( B ) After 40 h of FCS reduction from 10% to 0.4%, hepcidin transcripts were hardly detectable by RPA in HepG2 cells, whereas hypoxic IGFBP1 induction was not affected. Representative of three independent experiments. U6sn RNA served as loading control. ( C ) Exposure of Huh7 cells to protein kinase inhibitors revealed that the pan kinase inhibitor staurosporine (stauro; 0.5 µM) and the PI3 kinase inhibitor LY294002 (LY; 10 µM) reduced hepcidin expression similar to serum deprivation, whereas the p38 SAP kinase inhibitor SB202190 (SB; 10 µM) had no effect and the MEK1/2 inhibitor UO126 (1 µM) even increased HAMP/18S ratios. Data are results of qRT PCR analyses and given as means of three independent experiments±SEM; *p
    Figure Legend Snippet: Response of hepcidin transcript levels to serum deprivation and protein kinase inhibition. ( A ) Serum withdrawal rapidly decreased hepcidin transcript levels in Huh7 cells. ( B ) After 40 h of FCS reduction from 10% to 0.4%, hepcidin transcripts were hardly detectable by RPA in HepG2 cells, whereas hypoxic IGFBP1 induction was not affected. Representative of three independent experiments. U6sn RNA served as loading control. ( C ) Exposure of Huh7 cells to protein kinase inhibitors revealed that the pan kinase inhibitor staurosporine (stauro; 0.5 µM) and the PI3 kinase inhibitor LY294002 (LY; 10 µM) reduced hepcidin expression similar to serum deprivation, whereas the p38 SAP kinase inhibitor SB202190 (SB; 10 µM) had no effect and the MEK1/2 inhibitor UO126 (1 µM) even increased HAMP/18S ratios. Data are results of qRT PCR analyses and given as means of three independent experiments±SEM; *p

    Techniques Used: Inhibition, Recombinase Polymerase Amplification, Expressing, Quantitative RT-PCR

    Related Articles

    Incubation:

    Article Title: Brx Mediates the Response of Lymphocytes to Osmotic Stress Through the Activation of NFAT5
    Article Snippet: .. In some experiments, Jurkat cells were incubated with the p38 MAPK inhibitor SB202190 (2 μM) or the MEK1 inhibitor PD98059 (10 μM) (Sigma-Aldrich) in the absence or presence of 100 mM NaCl. .. After 8 hours of incubation, total RNA was harvested for real-time RT-PCR analysis.

    other:

    Article Title: Preferential Signaling and Induction of Allergy-promoting Lymphokines Upon Weak Stimulation of the High Affinity IgE Receptor on Mast Cells
    Article Snippet: However, another analyzed gene, IL-13, which responded to intermediate Ag concentrations or receptor occupancy, was not as effectively inhibited (∼23–38%) by SB202190 or PD98059.

    Article Title: The anti-tumor efficacy of 2-deoxyglucose and D-allose are enhanced with p38 inhibition in pancreatic and ovarian cell lines
    Article Snippet: Because SB202190 was kept at a constant dose during cell treatments, combination indices were not calculated.

    Activity Assay:

    Article Title: The anti-tumor efficacy of 2-deoxyglucose and D-allose are enhanced with p38 inhibition in pancreatic and ovarian cell lines
    Article Snippet: .. We also investigated the ability of SB202190 to modulate HRE activity (grey bars). ..

    Inhibition:

    Article Title: The anti-tumor efficacy of 2-deoxyglucose and D-allose are enhanced with p38 inhibition in pancreatic and ovarian cell lines
    Article Snippet: .. SB202190 enhances 2-DG and D-allose mediated PARP cleavage To investigate if p38 MAPK inhibition sensitizes cancer cells to apoptosis we pre-treated MIA PaCa-2 cells with SB202190 for 2 hours and then added 10 mM 2-DG or 10 mM D-allose (with no washout of SB202190) for 24 hours. .. Western blot analysis of whole cell lysates was performed and the blots probed for cleaved and total PARP (Figure ).

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    Millipore mapk inhibitors sb202190
    Effect of <t>MAPK</t> inhibitors on ICAM-1 and VCAM-1 expressions. ( a ) HT29 cells were pretreated with <t>SB202190</t> or SP600125 (10 μ M ) for 30 min and then incubated from time 0 to 8 h. At the time indicated, cells were processed
    Mapk Inhibitors Sb202190, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 157 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mapk inhibitors sb202190/product/Millipore
    Average 99 stars, based on 157 article reviews
    Price from $9.99 to $1999.99
    mapk inhibitors sb202190 - by Bioz Stars, 2020-09
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    Effect of MAPK inhibitors on ICAM-1 and VCAM-1 expressions. ( a ) HT29 cells were pretreated with SB202190 or SP600125 (10 μ M ) for 30 min and then incubated from time 0 to 8 h. At the time indicated, cells were processed

    Journal:

    Article Title: Celecoxib decreases expression of the adhesion molecules ICAM-1 and VCAM-1 in a colon cancer cell line (HT29)

    doi: 10.1038/sj.bjp.0707634

    Figure Lengend Snippet: Effect of MAPK inhibitors on ICAM-1 and VCAM-1 expressions. ( a ) HT29 cells were pretreated with SB202190 or SP600125 (10 μ M ) for 30 min and then incubated from time 0 to 8 h. At the time indicated, cells were processed

    Article Snippet: The MAPK inhibitors SB202190, PD98059 and SP600125 were from Calbiochem (San Diego, CA).

    Techniques: Incubation

    Activation of NF-κB by BPDE and the effect of TPA and SB202190 on BPDE-induced NF-κB activation. NF-κB activation corresponding to luciferase activity in the extracts of Cl41 cells harboring NFκB-responsive luciferase reporter

    Journal:

    Article Title: Attenuation of BPDE-induced p53 accumulation by TPA is associated with a decrease in stability and phosphorylation of p53 and down-regulation of NF-?B activation: Role of p38 MAP kinase

    doi: 10.1093/carcin/bgi247

    Figure Lengend Snippet: Activation of NF-κB by BPDE and the effect of TPA and SB202190 on BPDE-induced NF-κB activation. NF-κB activation corresponding to luciferase activity in the extracts of Cl41 cells harboring NFκB-responsive luciferase reporter

    Article Snippet: Our observation of significant attenuation of BPDE-induced p53 accumulation in cells treated with U0126 (MEK inhibitor) or SB202190 (p38 MAPK inhibitor) indicates the possible role of ERKs and p38 MAPK in p53 accumulation.

    Techniques: Activation Assay, Luciferase, Activity Assay

    Inhibition of CCL2 and CCL7 production by single MAPK inhibitors Rat astrocytes were pre-treated with 10 µM of selective inhibitors of MAPK pathways (SB203580 and SB202190 for p38, U0126 for ERK1/2, or SP600125 for JNK1/2) or control compounds (SB202474, U0124, or JNK ctr- B-F only) for 20 min before addition of 2.5 ng/ml IL-1β or 25 ng/ml TNF-α for 30 min (A), 24 hr (B,E,F) or 6 hr (C,D). Inhibition of specific MAPK pathways was analyzed by Western blots of cell lysates with antibodies against the activated (phosphorylated) form of a substrate downstream of the inhibitor target: phospho MK2 (for p38 inhibitor SB203580), phospho ERK1/2 (for MEK1/2 inhibitor U0126), phospho c-jun (for JNK1/2 inhibitor SP600125), and β-Actin loading control (A). Cell viability was measured by MTS assay (B). After stimulation of cells with IL-1β or TNF-α for 24 hr, MTS reagent was added into each well, cultures were incubated for an additional hr, and the absorbance at 490 nm was measured as described in Methods. Levels of CCL2 (C,D) or CCL7 (E,F) in conditioned media from astrocytes stimulated with IL-1β (C,E) and TNF-α (D,F) were determined by ELISA as described in Methods. Data are expressed as % IL-1β alone or % TNF-α alone. Data are mean ± SEM from triplicate determinations and show a representative 1 of 3 independent experiments (A,B), or are the mean ± SEM of 9–11 independent experiments of triplicate determinations (C–F). Data were analyzed by one way ANOVA followed by Dunnett’s multiple comparison test, *p

    Journal: Brain research

    Article Title: Inflammatory cytokines stimulate the chemokines CCL2/MCP-1 and CCL7/MCP-7 through NF?B and MAPK dependent pathways in rat astrocytes

    doi: 10.1016/j.brainres.2009.06.081

    Figure Lengend Snippet: Inhibition of CCL2 and CCL7 production by single MAPK inhibitors Rat astrocytes were pre-treated with 10 µM of selective inhibitors of MAPK pathways (SB203580 and SB202190 for p38, U0126 for ERK1/2, or SP600125 for JNK1/2) or control compounds (SB202474, U0124, or JNK ctr- B-F only) for 20 min before addition of 2.5 ng/ml IL-1β or 25 ng/ml TNF-α for 30 min (A), 24 hr (B,E,F) or 6 hr (C,D). Inhibition of specific MAPK pathways was analyzed by Western blots of cell lysates with antibodies against the activated (phosphorylated) form of a substrate downstream of the inhibitor target: phospho MK2 (for p38 inhibitor SB203580), phospho ERK1/2 (for MEK1/2 inhibitor U0126), phospho c-jun (for JNK1/2 inhibitor SP600125), and β-Actin loading control (A). Cell viability was measured by MTS assay (B). After stimulation of cells with IL-1β or TNF-α for 24 hr, MTS reagent was added into each well, cultures were incubated for an additional hr, and the absorbance at 490 nm was measured as described in Methods. Levels of CCL2 (C,D) or CCL7 (E,F) in conditioned media from astrocytes stimulated with IL-1β (C,E) and TNF-α (D,F) were determined by ELISA as described in Methods. Data are expressed as % IL-1β alone or % TNF-α alone. Data are mean ± SEM from triplicate determinations and show a representative 1 of 3 independent experiments (A,B), or are the mean ± SEM of 9–11 independent experiments of triplicate determinations (C–F). Data were analyzed by one way ANOVA followed by Dunnett’s multiple comparison test, *p

    Article Snippet: Inhibitors of MAPK pathways, SB203580 and SB202190 (p38 MAPK inhibitors), U0126 (MEK inhibitor), SP600125 (JNK inhibitor) and control compounds SB202474 (negative control for p38 MAPK inhibitor), U0124 (negative control for MEK inhibitor), and JNK Inhibitor II negative control (JNK ctr) (all from Calbiochem, La Jolla, CA) were prepared as 30 mM stocks in dimethysulfoxide (DMSO; Sigma, cell culture grade) and used at the concentrations indicated.

    Techniques: Inhibition, Western Blot, MTS Assay, Incubation, Enzyme-linked Immunosorbent Assay

    Transactivation of EGFR by LPS induces COX-2 expression in IEC-6 cells in an MMP- and p38-dependent fashion. A) IEC-6 cells were treated with LPS (2 µg/mL) for the indicated time or with EGF (10 ng/mL) for 5 minutes. EGFR immunoprecipitates were assayed for P-EGFR by Western blot analysis. B) Western blot analysis of cells treated with LPS (2 µg/mL) or EGF (10 ng/mL) for 24 hours in the presence or absence of the EGFR kinase inhibitor AG1478 (1 µM). C) IEC-6 cells were stimulated with LPS (2 µg/mL) for 24 hours in the presence or absence of the Src family kinase inhibitor CGP77675 (2 µM) or the MMP inhibitor GM6001 (50 µM). D) IEC-6 cells were stimulated with LPS (2 µg/mL) for 15 minutes in the presence or absence of CGP77675 (2 µM), GM6001 (50 µM), or p38 MAPK inhibitor SB202190 (10 µM). Single asterisks indicate significant differences from control. Double asterisks indicate significant differences between two bracketed conditions.

    Journal: PLoS ONE

    Article Title: Transactivation of EGFR by LPS Induces COX-2 Expression in Enterocytes

    doi: 10.1371/journal.pone.0038373

    Figure Lengend Snippet: Transactivation of EGFR by LPS induces COX-2 expression in IEC-6 cells in an MMP- and p38-dependent fashion. A) IEC-6 cells were treated with LPS (2 µg/mL) for the indicated time or with EGF (10 ng/mL) for 5 minutes. EGFR immunoprecipitates were assayed for P-EGFR by Western blot analysis. B) Western blot analysis of cells treated with LPS (2 µg/mL) or EGF (10 ng/mL) for 24 hours in the presence or absence of the EGFR kinase inhibitor AG1478 (1 µM). C) IEC-6 cells were stimulated with LPS (2 µg/mL) for 24 hours in the presence or absence of the Src family kinase inhibitor CGP77675 (2 µM) or the MMP inhibitor GM6001 (50 µM). D) IEC-6 cells were stimulated with LPS (2 µg/mL) for 15 minutes in the presence or absence of CGP77675 (2 µM), GM6001 (50 µM), or p38 MAPK inhibitor SB202190 (10 µM). Single asterisks indicate significant differences from control. Double asterisks indicate significant differences between two bracketed conditions.

    Article Snippet: Specific inhibitors were from the following sources: EGFR kinase inhibitor AG1478, MMP inhibitor GM6001, p38 MAPK inhibitor SB202190 were purchased from EMD Chemicals (Gibbstown, NJ); the ERK1/2 inhibitor U0126 was purchased from Cell Signaling Technology (Boston, MA); and the selective COX-2 inhibitor Celecoxib was purchased from Sigma (St. Louis, MO).

    Techniques: Expressing, Western Blot

    ERK and Src, but not p38, are required for EGFR-mediated induction of COX-2. A) IEC-6 cells were treated with LPS (2 µg/mL) for 15 minutes or with EGF (10 ng/mL) for 5 minutes in the presence or absence of the EGFR kinase inhibitor AG1478 (1 µM). Western blot analysis of P-p38 MAPK showed no significant difference in p38 activation in the presence of EGFR inhibition. B) IEC-6 cells stimulated with LPS (2 µg/mL) for 15 minutes or with EGF (10 ng/mL) for 5 minutes in the presence or absence of AG1478 (1 µM). C) IEC-6 cells were treated with LPS (2 µg/mL) for 24 hours or with EGF (10 ng/mL) for 5 minutes in the presence or absence of the ERK1/2 inhibitor U0126 (10 µM) or the p38 inhibitor SB202190 (10 µM) as shown, and COX-2 expression was determined using Western blot analysis. D) IEC-6 cells were treated with EGF (10 ng/mL) for 5 minutes in the presence or absence of the Src family kinase inhibitor CGP77675 (2 µM) and analyzed for P-ERK activation using Western blot analysis. Src inhibition had no effect on EGF-induced P-ERK (p = 0.7). IEC-6 cells were also treated with EGF (10 ng/mL) for 5 minutes in the presence or absence of the ERK kinase inhibitor U1026 (10 µM) and analyzed for P-Src activation using Western blot analysis. ERK inhibition had no effect on EGF-induced P-Src activation (p = 0.17). Single asterisks indicate significant differences from control. Double asterisks indicate significant differences between two bracketed conditions.

    Journal: PLoS ONE

    Article Title: Transactivation of EGFR by LPS Induces COX-2 Expression in Enterocytes

    doi: 10.1371/journal.pone.0038373

    Figure Lengend Snippet: ERK and Src, but not p38, are required for EGFR-mediated induction of COX-2. A) IEC-6 cells were treated with LPS (2 µg/mL) for 15 minutes or with EGF (10 ng/mL) for 5 minutes in the presence or absence of the EGFR kinase inhibitor AG1478 (1 µM). Western blot analysis of P-p38 MAPK showed no significant difference in p38 activation in the presence of EGFR inhibition. B) IEC-6 cells stimulated with LPS (2 µg/mL) for 15 minutes or with EGF (10 ng/mL) for 5 minutes in the presence or absence of AG1478 (1 µM). C) IEC-6 cells were treated with LPS (2 µg/mL) for 24 hours or with EGF (10 ng/mL) for 5 minutes in the presence or absence of the ERK1/2 inhibitor U0126 (10 µM) or the p38 inhibitor SB202190 (10 µM) as shown, and COX-2 expression was determined using Western blot analysis. D) IEC-6 cells were treated with EGF (10 ng/mL) for 5 minutes in the presence or absence of the Src family kinase inhibitor CGP77675 (2 µM) and analyzed for P-ERK activation using Western blot analysis. Src inhibition had no effect on EGF-induced P-ERK (p = 0.7). IEC-6 cells were also treated with EGF (10 ng/mL) for 5 minutes in the presence or absence of the ERK kinase inhibitor U1026 (10 µM) and analyzed for P-Src activation using Western blot analysis. ERK inhibition had no effect on EGF-induced P-Src activation (p = 0.17). Single asterisks indicate significant differences from control. Double asterisks indicate significant differences between two bracketed conditions.

    Article Snippet: Specific inhibitors were from the following sources: EGFR kinase inhibitor AG1478, MMP inhibitor GM6001, p38 MAPK inhibitor SB202190 were purchased from EMD Chemicals (Gibbstown, NJ); the ERK1/2 inhibitor U0126 was purchased from Cell Signaling Technology (Boston, MA); and the selective COX-2 inhibitor Celecoxib was purchased from Sigma (St. Louis, MO).

    Techniques: Western Blot, Activation Assay, Inhibition, Expressing