p38 inhibitor sb202190  (Millipore)


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    Structured Review

    Millipore p38 inhibitor sb202190
    P38 Inhibitor Sb202190, supplied by Millipore, used in various techniques. Bioz Stars score: 98/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p38 inhibitor sb202190/product/Millipore
    Average 98 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    p38 inhibitor sb202190 - by Bioz Stars, 2020-02
    98/100 stars

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    Concentration Assay:

    Article Title: The contribution of c-Jun N-terminal kinase activation and subsequent Bcl-2 phosphorylation to apoptosis induction in human B-cells is dependent on the mode of action of specific stresses
    Article Snippet: The JNK inhibitor SP600125 (SP6; Anthra[1,9- cd ]pyrazol-6(2 H )-one-1,9-pyrazoloanthron), JNK inhibitor II (a structural but inactive analogue of SP6 serving as a negative control; N1-methyl-1,9,pyrazoloanthrone), JNK inhibitor V, (a structurally unrelated JNK inhibitor, 1,3,-benzothiazole-2-yl-(2-(2-(3-pyridinyl)ethyl)amino)-4-pyrimidinyl acetonitrile), the ERK inhibitor U0126, and p38 inhibitor SB202190 (SB2), were obtained from Calbiochem Inc. All inhibitors were dissolved in DMSO. .. Additional experiments with the JNK inhibitor V were performed (data not shown) in which a working concentration of 10 µM was found to be adequate to inhibit JNK-activity, as measured by induction of c-Jun protein without increasing baseline levels of apoptosis/necrosis in the cells.

    Negative Control:

    Article Title: The contribution of c-Jun N-terminal kinase activation and subsequent Bcl-2 phosphorylation to apoptosis induction in human B-cells is dependent on the mode of action of specific stresses
    Article Snippet: .. The JNK inhibitor SP600125 (SP6; Anthra[1,9- cd ]pyrazol-6(2 H )-one-1,9-pyrazoloanthron), JNK inhibitor II (a structural but inactive analogue of SP6 serving as a negative control; N1-methyl-1,9,pyrazoloanthrone), JNK inhibitor V, (a structurally unrelated JNK inhibitor, 1,3,-benzothiazole-2-yl-(2-(2-(3-pyridinyl)ethyl)amino)-4-pyrimidinyl acetonitrile), the ERK inhibitor U0126, and p38 inhibitor SB202190 (SB2), were obtained from Calbiochem Inc. All inhibitors were dissolved in DMSO. ..

    Blocking Assay:

    Article Title: The contribution of c-Jun N-terminal kinase activation and subsequent Bcl-2 phosphorylation to apoptosis induction in human B-cells is dependent on the mode of action of specific stresses
    Article Snippet: The JNK inhibitor SP600125 (SP6; Anthra[1,9- cd ]pyrazol-6(2 H )-one-1,9-pyrazoloanthron), JNK inhibitor II (a structural but inactive analogue of SP6 serving as a negative control; N1-methyl-1,9,pyrazoloanthrone), JNK inhibitor V, (a structurally unrelated JNK inhibitor, 1,3,-benzothiazole-2-yl-(2-(2-(3-pyridinyl)ethyl)amino)-4-pyrimidinyl acetonitrile), the ERK inhibitor U0126, and p38 inhibitor SB202190 (SB2), were obtained from Calbiochem Inc. All inhibitors were dissolved in DMSO. .. Thus, concentrations of inhibitors in their range of 10 – 20 µM were necessary to block the activities of the respective kinases in the absence of measurable, non-specific, effects on other kinases.

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    Millipore sb202190
    TcdB, but not latrunculin B, induced IL-8 secretion in HMC-1 cells. TcdB (6 nM) induced the secretion of 605 ± 58 ng per 10 6 cells over 5 h of treatment, whereas controls showed a constitutive secretion of 29 ± 28 ng per 10 6 cells. IL-8 secretion induced by TcdB was prevented in the presence of the p38 MAPK inhibitor <t>SB202190</t> (58 ± 21 ng per 10 6 cells). In contrast to TcdB, latrunculin B (Lat B; 2 μg/ml) did not induce a strong increase in IL-8 secretion compared to that in controls (52 ± 2 ng per 10 6 cells). Shown are mean values ± standard deviations from six separate experiments.
    Sb202190, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 26 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/sb202190/product/Millipore
    Average 95 stars, based on 26 article reviews
    Price from $9.99 to $1999.99
    sb202190 - by Bioz Stars, 2020-02
    95/100 stars
      Buy from Supplier

    95
    Millipore p38 mapk inhibitor sb202190
    Model for PV pathogenicity. Monoclonal pathogenic antibodies, such as AK23 and monovalent PV mAbs (scFv) cloned from patients, cause loss of adhesion primarily through steric hindrance, which does not require signaling through <t>p38</t> <t>MAPK.</t> In contrast, PV IgG induce two separate pathogenic events. In addition to the steric hindrance caused by a portion of antibodies contained in PV IgG, the polyclonal nature of PV IgG causes clustering and endocytosis of Dsg3 in a p38 MAPK dependent manner.
    P38 Mapk Inhibitor Sb202190, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p38 mapk inhibitor sb202190/product/Millipore
    Average 95 stars, based on 8 article reviews
    Price from $9.99 to $1999.99
    p38 mapk inhibitor sb202190 - by Bioz Stars, 2020-02
    95/100 stars
      Buy from Supplier

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    TcdB, but not latrunculin B, induced IL-8 secretion in HMC-1 cells. TcdB (6 nM) induced the secretion of 605 ± 58 ng per 10 6 cells over 5 h of treatment, whereas controls showed a constitutive secretion of 29 ± 28 ng per 10 6 cells. IL-8 secretion induced by TcdB was prevented in the presence of the p38 MAPK inhibitor SB202190 (58 ± 21 ng per 10 6 cells). In contrast to TcdB, latrunculin B (Lat B; 2 μg/ml) did not induce a strong increase in IL-8 secretion compared to that in controls (52 ± 2 ng per 10 6 cells). Shown are mean values ± standard deviations from six separate experiments.

    Journal: Infection and Immunity

    Article Title: Clostridium difficile Toxins A and B Directly Stimulate Human Mast Cells ▿

    doi: 10.1128/IAI.00195-07

    Figure Lengend Snippet: TcdB, but not latrunculin B, induced IL-8 secretion in HMC-1 cells. TcdB (6 nM) induced the secretion of 605 ± 58 ng per 10 6 cells over 5 h of treatment, whereas controls showed a constitutive secretion of 29 ± 28 ng per 10 6 cells. IL-8 secretion induced by TcdB was prevented in the presence of the p38 MAPK inhibitor SB202190 (58 ± 21 ng per 10 6 cells). In contrast to TcdB, latrunculin B (Lat B; 2 μg/ml) did not induce a strong increase in IL-8 secretion compared to that in controls (52 ± 2 ng per 10 6 cells). Shown are mean values ± standard deviations from six separate experiments.

    Article Snippet: TcdB- and latrunculin-induced hexosaminidase release was reduced a great extent by coincubating the cells with SB202190 (Fig. ).

    Techniques:

    (A) Activation of p38 MAPK and ERK1/2 in response to the reorganization of the actin cytoskeleton. Cells were treated with TcdB (6 nM) and latrunculin B (Lat B; 2 μg/ml) for 1 h in the absence or presence of 3 μM bafilomycin A1. Immunoblot analysis shows the phosphorylation of p38 MAPK (p-p38) (upper panel) and ERK1/2 (p-ERK1/2) (middle panel). Beta-actin, shown in the lower panel, serves as a control for identical protein loads. (B) Effect of p38 MAPK inhibition by SB202190 (10 μM) on hexosaminidase release induced by TcdB (6 nM) or latrunculin B (2 μg/ml). In comparison to what occurred in control cells (100% ± 34%), the TcdB-induced (288% ± 8%) and the latrunculin B-induced (196% ± 23%) release of hexosaminidase was partially reduced by the p38 MAPK inhibitor SB202190 (TcdB, 236% ± 39%; latrunculin B, 133% ± 11%). Shown are mean values ± standard deviations from three separate experiments.

    Journal: Infection and Immunity

    Article Title: Clostridium difficile Toxins A and B Directly Stimulate Human Mast Cells ▿

    doi: 10.1128/IAI.00195-07

    Figure Lengend Snippet: (A) Activation of p38 MAPK and ERK1/2 in response to the reorganization of the actin cytoskeleton. Cells were treated with TcdB (6 nM) and latrunculin B (Lat B; 2 μg/ml) for 1 h in the absence or presence of 3 μM bafilomycin A1. Immunoblot analysis shows the phosphorylation of p38 MAPK (p-p38) (upper panel) and ERK1/2 (p-ERK1/2) (middle panel). Beta-actin, shown in the lower panel, serves as a control for identical protein loads. (B) Effect of p38 MAPK inhibition by SB202190 (10 μM) on hexosaminidase release induced by TcdB (6 nM) or latrunculin B (2 μg/ml). In comparison to what occurred in control cells (100% ± 34%), the TcdB-induced (288% ± 8%) and the latrunculin B-induced (196% ± 23%) release of hexosaminidase was partially reduced by the p38 MAPK inhibitor SB202190 (TcdB, 236% ± 39%; latrunculin B, 133% ± 11%). Shown are mean values ± standard deviations from three separate experiments.

    Article Snippet: TcdB- and latrunculin-induced hexosaminidase release was reduced a great extent by coincubating the cells with SB202190 (Fig. ).

    Techniques: Activation Assay, Inhibition

    Release of prostaglandins. Treatment of HMC-1 cells with either TcdB (6 nM) or latrunculin B (Lat B; 2 μg/ml) for 5 h induced the synthesis of PGE 2 (A) and PGD 2 (B). The formation of prostaglandins was completely abolished by the preincubation of cells with the p38 MAPK inhibitor SB202190 (10 μM). Due to the high standard deviation of PGD 2 synthesis induced by latrunculin B, the effect of SB202190 was not considered significant (n.s.). (C) Effect of PGE 2 (1 ng/ml) on the hexosaminidase release of HMC-1 cells. (D) Inhibition of the cyclooxygenase by 10 μM indomethacin (Indo) only partially reduced TcdB-induced hexosaminidase release. All values are means ± standard deviations from three separate experiments. Significant effects ( P

    Journal: Infection and Immunity

    Article Title: Clostridium difficile Toxins A and B Directly Stimulate Human Mast Cells ▿

    doi: 10.1128/IAI.00195-07

    Figure Lengend Snippet: Release of prostaglandins. Treatment of HMC-1 cells with either TcdB (6 nM) or latrunculin B (Lat B; 2 μg/ml) for 5 h induced the synthesis of PGE 2 (A) and PGD 2 (B). The formation of prostaglandins was completely abolished by the preincubation of cells with the p38 MAPK inhibitor SB202190 (10 μM). Due to the high standard deviation of PGD 2 synthesis induced by latrunculin B, the effect of SB202190 was not considered significant (n.s.). (C) Effect of PGE 2 (1 ng/ml) on the hexosaminidase release of HMC-1 cells. (D) Inhibition of the cyclooxygenase by 10 μM indomethacin (Indo) only partially reduced TcdB-induced hexosaminidase release. All values are means ± standard deviations from three separate experiments. Significant effects ( P

    Article Snippet: TcdB- and latrunculin-induced hexosaminidase release was reduced a great extent by coincubating the cells with SB202190 (Fig. ).

    Techniques: Standard Deviation, Inhibition

    Cdt2 phosphorylation after UV irradiation is caffeine- and MAP kinase-inhibitor sensitive. A. HeLa cells synchronized in the G1 phase were treated with the indicated inhibitors for 2 h and UV-irradiated (+) or not (−). Cell extract was blotted with Cdt1 and Cdt2 antibodies. Inhibitors used were: ERKi, U0126; JNKi, SP600125; p38i, SB202190. The asterisk indicates a non-specific band, and used as a loading control. B. Asynchronously growing HeLa cells were treated with the indicated MAP kinase inhibitors and UV-irradiated (+) or not. One hour later, cells were examined for Cdt2 phosphorylation levels and Cdt1 protein levels. Cdt2 phosphorylation levels were examined using Phos-tag gel. C. Target specificity of inhibitors. Activation of each MAP kinase was examined using specific phosphopeptide antibodies (Erk1 and 2, JNK or p38) before (−) and after (+) UV-irradiation (C-1 and 2). Cells, treated or not with the indicated inhibitors for 2 h, were UV-irradiated or not. One hour later, cell extracts were prepared and their phosphorylation levels of ERK (Erk1 and Erk2), Jun, and MAPKAPK2 (MK2) were examined(C-2). Note that U0126 inhibits the ERK pathway by inhibiting ERK1-activating kinases MEK1 and MEK2. Jun is a JNK substrate and MAPKAPK2 is a p38 substrate. Arrow in MK2 Western blotting indicates the phosphorylated form of MK2. The asterisk indicates a non-specific band.

    Journal: PLoS ONE

    Article Title: Checkpoint Kinase ATR Phosphorylates Cdt2, a Substrate Receptor of CRL4 Ubiquitin Ligase, and Promotes the Degradation of Cdt1 following UV Irradiation

    doi: 10.1371/journal.pone.0046480

    Figure Lengend Snippet: Cdt2 phosphorylation after UV irradiation is caffeine- and MAP kinase-inhibitor sensitive. A. HeLa cells synchronized in the G1 phase were treated with the indicated inhibitors for 2 h and UV-irradiated (+) or not (−). Cell extract was blotted with Cdt1 and Cdt2 antibodies. Inhibitors used were: ERKi, U0126; JNKi, SP600125; p38i, SB202190. The asterisk indicates a non-specific band, and used as a loading control. B. Asynchronously growing HeLa cells were treated with the indicated MAP kinase inhibitors and UV-irradiated (+) or not. One hour later, cells were examined for Cdt2 phosphorylation levels and Cdt1 protein levels. Cdt2 phosphorylation levels were examined using Phos-tag gel. C. Target specificity of inhibitors. Activation of each MAP kinase was examined using specific phosphopeptide antibodies (Erk1 and 2, JNK or p38) before (−) and after (+) UV-irradiation (C-1 and 2). Cells, treated or not with the indicated inhibitors for 2 h, were UV-irradiated or not. One hour later, cell extracts were prepared and their phosphorylation levels of ERK (Erk1 and Erk2), Jun, and MAPKAPK2 (MK2) were examined(C-2). Note that U0126 inhibits the ERK pathway by inhibiting ERK1-activating kinases MEK1 and MEK2. Jun is a JNK substrate and MAPKAPK2 is a p38 substrate. Arrow in MK2 Western blotting indicates the phosphorylated form of MK2. The asterisk indicates a non-specific band.

    Article Snippet: MAP kinase inhibitors were used at the following concentrations: ERK inhibitor U0126 (Calbiochem) at 10 µM, JNK inhibitor II (SP600125, Calbiochem) at 30 µM and p38 inhibitor SB202190 (Calbiochem) at 20 µM.

    Techniques: Irradiation, Activation Assay, Western Blot

    Model for PV pathogenicity. Monoclonal pathogenic antibodies, such as AK23 and monovalent PV mAbs (scFv) cloned from patients, cause loss of adhesion primarily through steric hindrance, which does not require signaling through p38 MAPK. In contrast, PV IgG induce two separate pathogenic events. In addition to the steric hindrance caused by a portion of antibodies contained in PV IgG, the polyclonal nature of PV IgG causes clustering and endocytosis of Dsg3 in a p38 MAPK dependent manner.

    Journal: PLoS ONE

    Article Title: Signaling Dependent and Independent Mechanisms in Pemphigus Vulgaris Blister Formation

    doi: 10.1371/journal.pone.0050696

    Figure Lengend Snippet: Model for PV pathogenicity. Monoclonal pathogenic antibodies, such as AK23 and monovalent PV mAbs (scFv) cloned from patients, cause loss of adhesion primarily through steric hindrance, which does not require signaling through p38 MAPK. In contrast, PV IgG induce two separate pathogenic events. In addition to the steric hindrance caused by a portion of antibodies contained in PV IgG, the polyclonal nature of PV IgG causes clustering and endocytosis of Dsg3 in a p38 MAPK dependent manner.

    Article Snippet: The p38 MAPK inhibitor SB202190 was purchased from Calbiochem (La Jolla, CA) and used at 20 µM.

    Techniques:

    Tumor necrosis factor-α (TNFα) mRNA and TNFα protein (mTNFα plus sTNFα) in HAPI cells pretreated with 10 μM SB202190 for 30 min prior to addition of lipopolysaccharide (LPS) determined by RT–PCR ( a ) and western blot ( c ). The amount of mRNA was quantified by relative optical density ( b ) and the sum of the 17 and 26 kDa protein bands quantified by chemiluminescence ( d ), normalized to β-actin mRNA and protein levels, respectively. sTNFα released in the culture medium by ELISA ( e ). p-p38 and p38 protein (western blot) in HAPI cells transduced with QHGFP or QHIL10 and exposed the LPS ( f ). Ratio of p-p38 to p38-determined chemiluminescence ( g ). Data presented represent the results of three independent experiments. Mean±s.e.m.; * P

    Journal: Gene therapy

    Article Title: HSV-mediated transfer of interleukin-10 reduces inflammatory pain through modulation of membrane tumor necrosis factor α in spinal cord microglia

    doi: 10.1038/sj.gt.3303054

    Figure Lengend Snippet: Tumor necrosis factor-α (TNFα) mRNA and TNFα protein (mTNFα plus sTNFα) in HAPI cells pretreated with 10 μM SB202190 for 30 min prior to addition of lipopolysaccharide (LPS) determined by RT–PCR ( a ) and western blot ( c ). The amount of mRNA was quantified by relative optical density ( b ) and the sum of the 17 and 26 kDa protein bands quantified by chemiluminescence ( d ), normalized to β-actin mRNA and protein levels, respectively. sTNFα released in the culture medium by ELISA ( e ). p-p38 and p38 protein (western blot) in HAPI cells transduced with QHGFP or QHIL10 and exposed the LPS ( f ). Ratio of p-p38 to p38-determined chemiluminescence ( g ). Data presented represent the results of three independent experiments. Mean±s.e.m.; * P

    Article Snippet: In the LPS experiments, HAPI cells were treated with LPS (1 μg ml−1 , Sigma-Aldrich, St Louis, MO, USA) for 6 h. In some experiments 10 μM of p38 MAPK inhibitor SB202190 (Calbiochem, La Jolla, CA, USA) was added 30 min prior to LPS treatment.

    Techniques: Reverse Transcription Polymerase Chain Reaction, Western Blot, Enzyme-linked Immunosorbent Assay, Transduction