sb202190  (Tocris)

 
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    Name:
    SB 202190
    Description:
    Potent selective inhibitor of p38 MAPK
    Catalog Number:
    1264
    Price:
    None
    Category:
    p38 MAPK Inhibitors p38 MAPK MAPK Family Kinases Enzymes Pharmacology
    Purity:
    ≥99% (HPLC)
    Formula:
    4-[4-(4-Fluorophenyl)-5-(4-pyridinyl)-1H-imidazol-2-yl]phenol
    Buy from Supplier


    Structured Review

    Tocris sb202190
    SB 202190
    Potent selective inhibitor of p38 MAPK
    https://www.bioz.com/result/sb202190/product/Tocris
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    sb202190 - by Bioz Stars, 2021-05
    93/100 stars

    Images

    1) Product Images from "The VGF-derived peptide TLQP-21 contributes to inflammatory and nerve injury-induced hypersensitivity"

    Article Title: The VGF-derived peptide TLQP-21 contributes to inflammatory and nerve injury-induced hypersensitivity

    Journal: Pain

    doi: 10.1016/j.pain.2014.03.012

    Spinal effects of exogenous TLQP-21 peptide. A , Intrathecal injection of TLQP-21 induced dose-dependent thermal hyperalgesia in the warm water immersion tail withdrawal test. B–D , The p38 MAPK inhibitor SB202190 ( B ), the cyclooxygenase (COX) inhibitor
    Figure Legend Snippet: Spinal effects of exogenous TLQP-21 peptide. A , Intrathecal injection of TLQP-21 induced dose-dependent thermal hyperalgesia in the warm water immersion tail withdrawal test. B–D , The p38 MAPK inhibitor SB202190 ( B ), the cyclooxygenase (COX) inhibitor

    Techniques Used: Injection

    2) Product Images from "Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190"

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190

    Journal: American Journal of Physiology - Cell Physiology

    doi: 10.1152/ajpcell.00184.2015

    IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.
    Figure Legend Snippet: IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.

    Techniques Used: Incubation, Immunocytochemistry, Staining, Live Cell Imaging

    SB202190
    Figure Legend Snippet: SB202190

    Techniques Used:

    Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.
    Figure Legend Snippet: Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.

    Techniques Used: Expressing, Incubation

    3) Product Images from "Direct activation of the mitochondrial calcium uniporter by natural plant flavonoids"

    Article Title: Direct activation of the mitochondrial calcium uniporter by natural plant flavonoids

    Journal: Biochemical Journal

    doi: 10.1042/BJ20040990

    Inhibition by Ru360 of the mitochondrial Ca 2+ uptake induced by kaempferol and SB202190 MM5 cells expressing mitochondrially targeted mutated aequorin reconstituted with coelenterazine n were permeabilized as described in the Experimental section. Then a Ca 2+ buffer containing 3.5 μM [Ca 2+ ] was perfused either in the absence (Control) or in the presence of 5 μM kaempferol, 10 μM SB202190, 5 μM kaempferol plus 100 nM Ru360 or 10 μM SB202190 plus 100 nM Ru360, as indicated. The experiments shown are representative of 3 similar ones of each type.
    Figure Legend Snippet: Inhibition by Ru360 of the mitochondrial Ca 2+ uptake induced by kaempferol and SB202190 MM5 cells expressing mitochondrially targeted mutated aequorin reconstituted with coelenterazine n were permeabilized as described in the Experimental section. Then a Ca 2+ buffer containing 3.5 μM [Ca 2+ ] was perfused either in the absence (Control) or in the presence of 5 μM kaempferol, 10 μM SB202190, 5 μM kaempferol plus 100 nM Ru360 or 10 μM SB202190 plus 100 nM Ru360, as indicated. The experiments shown are representative of 3 similar ones of each type.

    Techniques Used: Inhibition, Expressing

    Chemical structures of SB202190 and the natural flavonoids used in this study The structure of kaempferol shows the standard letter code used to name flavone rings.
    Figure Legend Snippet: Chemical structures of SB202190 and the natural flavonoids used in this study The structure of kaempferol shows the standard letter code used to name flavone rings.

    Techniques Used:

    4) Product Images from "Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190"

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190

    Journal: American Journal of Physiology - Cell Physiology

    doi: 10.1152/ajpcell.00184.2015

    IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.
    Figure Legend Snippet: IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.

    Techniques Used: Incubation, Immunocytochemistry, Staining, Live Cell Imaging

    SB202190
    Figure Legend Snippet: SB202190

    Techniques Used:

    Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.
    Figure Legend Snippet: Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.

    Techniques Used: Expressing, Incubation

    5) Product Images from "Intracellular pathways triggered by the selective FLT-1-agonist placental growth factor in vascular smooth muscle cells exposed to hypoxia"

    Article Title: Intracellular pathways triggered by the selective FLT-1-agonist placental growth factor in vascular smooth muscle cells exposed to hypoxia

    Journal:

    doi: 10.1038/sj.bjp.0706347

    (a) Effect of AG490, SB202190 and LY294002 on the P1GF-induced proliferation of cultured VSMCs. Growth-arrested and hypoxia-treated VSMCs were stimulated with 20 ng ml −1 P1GF in the presence and in the absence (control) of the
    Figure Legend Snippet: (a) Effect of AG490, SB202190 and LY294002 on the P1GF-induced proliferation of cultured VSMCs. Growth-arrested and hypoxia-treated VSMCs were stimulated with 20 ng ml −1 P1GF in the presence and in the absence (control) of the

    Techniques Used: Cell Culture

    Effect of SB202190 (10–1000 n M ) on the contractile response induced by P1GF in preparations exposed to hypoxia. Data are expressed as percent of P1GF-induced contraction (control). Means±s.e.m. of four preparations from four animals
    Figure Legend Snippet: Effect of SB202190 (10–1000 n M ) on the contractile response induced by P1GF in preparations exposed to hypoxia. Data are expressed as percent of P1GF-induced contraction (control). Means±s.e.m. of four preparations from four animals

    Techniques Used:

    6) Product Images from "Sodium Chloride Drives Autoimmune Disease by the Induction of Pathogenic Th17 Cells"

    Article Title: Sodium Chloride Drives Autoimmune Disease by the Induction of Pathogenic Th17 Cells

    Journal: Nature

    doi: 10.1038/nature11868

    The induction of Th17 cells by sodium chloride depends on p38/MAPK, NFAT5 and SGK1 a , Naive CD4 + cells were stimulated in the presence (NaCl) or absence (none) of additional 40 mM NaCl and were analysed by FACS for phosphorylated p38 (p-p38; n = 5). b, Naïve CD4 cells were differentiated into Th17 cells as indicated in the presence or absence of NaCl and SB202190 (p38i) and analysed by qRT-PCR as depicted in the bar graph (n=7) or by FACS (the left row shows cells differentiated in the absence of TGF-β1). c, Naïve CD4 cells were stimulated for 3h in the presence or absence of NaCl and SB202190 and analysed by qRT-PCR for NFAT5 (n=4). d, Cells were transduced with NFAT5 specific (shNFAT5) or control shRNA (control), stimulated like in b) and analysed by FACS. The bar graphs depict qRT-PCR analyses of NFAT5 , IL-17A and SLC5A3 (n=5). CCR6 was analysed by FACS (black histogram: control, grey histogram: shNFAT5, one representative experiment of four is shown). e, Cells were stimulated like in c), but analysed by qRT-PCR for SGK1 (n=4). f, Cells were transduced with a shRNA specific for SGK1 (shSGK1) or a control shRNA (control) and activated like in b), and analysed by FACS. Expression of SGK1 and IL-17A was determined by qRT-PCR (n=5). CCR6 was analysed by FACS (black histogram: control, grey histogram: shSGK1, one representative experiment of four is shown). g, Cells were cultured like in b), but in the presence or absence of the SGK1 inhibitor GSK650394 (SGK1i) and analysed by FACS. The bar graph shows qRT-PCR for IL-17A under similar conditions (n=5). FACS and qRT-PCR (relative expression) data depicted in bar graphs were normalised to controls.
    Figure Legend Snippet: The induction of Th17 cells by sodium chloride depends on p38/MAPK, NFAT5 and SGK1 a , Naive CD4 + cells were stimulated in the presence (NaCl) or absence (none) of additional 40 mM NaCl and were analysed by FACS for phosphorylated p38 (p-p38; n = 5). b, Naïve CD4 cells were differentiated into Th17 cells as indicated in the presence or absence of NaCl and SB202190 (p38i) and analysed by qRT-PCR as depicted in the bar graph (n=7) or by FACS (the left row shows cells differentiated in the absence of TGF-β1). c, Naïve CD4 cells were stimulated for 3h in the presence or absence of NaCl and SB202190 and analysed by qRT-PCR for NFAT5 (n=4). d, Cells were transduced with NFAT5 specific (shNFAT5) or control shRNA (control), stimulated like in b) and analysed by FACS. The bar graphs depict qRT-PCR analyses of NFAT5 , IL-17A and SLC5A3 (n=5). CCR6 was analysed by FACS (black histogram: control, grey histogram: shNFAT5, one representative experiment of four is shown). e, Cells were stimulated like in c), but analysed by qRT-PCR for SGK1 (n=4). f, Cells were transduced with a shRNA specific for SGK1 (shSGK1) or a control shRNA (control) and activated like in b), and analysed by FACS. Expression of SGK1 and IL-17A was determined by qRT-PCR (n=5). CCR6 was analysed by FACS (black histogram: control, grey histogram: shSGK1, one representative experiment of four is shown). g, Cells were cultured like in b), but in the presence or absence of the SGK1 inhibitor GSK650394 (SGK1i) and analysed by FACS. The bar graph shows qRT-PCR for IL-17A under similar conditions (n=5). FACS and qRT-PCR (relative expression) data depicted in bar graphs were normalised to controls.

    Techniques Used: FACS, Quantitative RT-PCR, Transduction, shRNA, Expressing, Cell Culture

    7) Product Images from "Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190"

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190

    Journal: American Journal of Physiology - Cell Physiology

    doi: 10.1152/ajpcell.00184.2015

    IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.
    Figure Legend Snippet: IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.

    Techniques Used: Incubation, Immunocytochemistry, Staining, Live Cell Imaging

    SB202190
    Figure Legend Snippet: SB202190

    Techniques Used:

    Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.
    Figure Legend Snippet: Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.

    Techniques Used: Expressing, Incubation

    8) Product Images from ""

    Article Title:

    Journal: Molecular Biology of the Cell

    doi: 10.1091/mbc.E06-02-0122

    The JNK signaling pathway is involved in the control of claudin-2, but not ZO-3 expression, independently of cingulin depletion and RhoA activity. (A) Immunoblotting analysis of cell lysates prepared from cingulin KD clone A treated either with solvent (dimethyl sulfoxide) or the MAPK/ERK inhibitor U0126 (15 μM), or the p38 kinase inhibitor SB202190 (20 μM), or the JNK inhibitor SP600125 (30 μM). Note the decrease in claudin-2 protein levels only in lysates from cells treated with the JNK inhibitor SP600125. Images are representative of two independent experiments, and the same results were obtained with cingulin KD clone B (our unpublished data). (B) Immunoblotting analysis of the effect of the JNK inhibitor SP600125 (30 μM) on the expression of cingulin, ZO-3, and claudin-2 in WT cells and control and cingulin KD clones. Note that SP600125 does not affect the protein expression levels of cingulin and ZO-3, but it reduces claudin-2 levels in WT cells and control and cingulin KD clones. Images are representative of two independent experiments. (C) Immunoblotting analysis of active JNK (phospho-JNK) (top) and total JNK (bottom), either in the absence (−) or in the presence (+) of the JNK inhibitor SP600125 (30 μM) in WT MDCK cells. Note that the JNK inhibitor decreases phospho-JNK levels by > 75%. Similar results were obtained for control and cingulin KD clones (our unpublished data). Images are representative of two independent experiments. (D) Immunoblotting analysis of JNK activity in WT cells and control and cingulin KD clones with or without (NT) coexpression of the dominant-negative RhoA mutant RhoAN19. Note that phospho-JNK levels are not affected either by cingulin depletion or by inhibition of RhoA. Images are representative of two independent experiments. (E) Immunoblotting analysis of claudin-2 levels in cingulin KD clones A and B, either untreated, or treated with the JNK inhibitor SP600125 (30 μM), with or without coexpression of RhoAN19. Note that claudin-2 levels in cells where JNK is inhibited are further decreased when RhoA is also inhibited.
    Figure Legend Snippet: The JNK signaling pathway is involved in the control of claudin-2, but not ZO-3 expression, independently of cingulin depletion and RhoA activity. (A) Immunoblotting analysis of cell lysates prepared from cingulin KD clone A treated either with solvent (dimethyl sulfoxide) or the MAPK/ERK inhibitor U0126 (15 μM), or the p38 kinase inhibitor SB202190 (20 μM), or the JNK inhibitor SP600125 (30 μM). Note the decrease in claudin-2 protein levels only in lysates from cells treated with the JNK inhibitor SP600125. Images are representative of two independent experiments, and the same results were obtained with cingulin KD clone B (our unpublished data). (B) Immunoblotting analysis of the effect of the JNK inhibitor SP600125 (30 μM) on the expression of cingulin, ZO-3, and claudin-2 in WT cells and control and cingulin KD clones. Note that SP600125 does not affect the protein expression levels of cingulin and ZO-3, but it reduces claudin-2 levels in WT cells and control and cingulin KD clones. Images are representative of two independent experiments. (C) Immunoblotting analysis of active JNK (phospho-JNK) (top) and total JNK (bottom), either in the absence (−) or in the presence (+) of the JNK inhibitor SP600125 (30 μM) in WT MDCK cells. Note that the JNK inhibitor decreases phospho-JNK levels by > 75%. Similar results were obtained for control and cingulin KD clones (our unpublished data). Images are representative of two independent experiments. (D) Immunoblotting analysis of JNK activity in WT cells and control and cingulin KD clones with or without (NT) coexpression of the dominant-negative RhoA mutant RhoAN19. Note that phospho-JNK levels are not affected either by cingulin depletion or by inhibition of RhoA. Images are representative of two independent experiments. (E) Immunoblotting analysis of claudin-2 levels in cingulin KD clones A and B, either untreated, or treated with the JNK inhibitor SP600125 (30 μM), with or without coexpression of RhoAN19. Note that claudin-2 levels in cells where JNK is inhibited are further decreased when RhoA is also inhibited.

    Techniques Used: Expressing, Activity Assay, Clone Assay, Dominant Negative Mutation, Mutagenesis, Inhibition

    9) Product Images from "Increased p38-MAPK is responsible for chemotherapy resistance in human gastric cancer cells"

    Article Title: Increased p38-MAPK is responsible for chemotherapy resistance in human gastric cancer cells

    Journal: BMC Cancer

    doi: 10.1186/1471-2407-8-375

    Inhibition of p38-MAPK impairs MDR1 expression and function of P-gp in SGC7901/VCR cells . SGC7901/VCR cells were treated with DMSO or SB202190 (10 μM). (A) Protein levels of P-gp were detected by Western-blot analysis. A representative example of an experiment that was repeated three times is shown. (B) SGC7901/VCR cells were treated with DMSO and SB202190. Expression of MDR1 mRNA was assessed by RT-PCR. β-actin mRNA levels were measured as positive internal controls. (C) The MDR1 mRNA expression levels were normalized to those of β-actin and are the means ± SD of at least three independent experiments. Significant differences are indicated by asterisks. *, P
    Figure Legend Snippet: Inhibition of p38-MAPK impairs MDR1 expression and function of P-gp in SGC7901/VCR cells . SGC7901/VCR cells were treated with DMSO or SB202190 (10 μM). (A) Protein levels of P-gp were detected by Western-blot analysis. A representative example of an experiment that was repeated three times is shown. (B) SGC7901/VCR cells were treated with DMSO and SB202190. Expression of MDR1 mRNA was assessed by RT-PCR. β-actin mRNA levels were measured as positive internal controls. (C) The MDR1 mRNA expression levels were normalized to those of β-actin and are the means ± SD of at least three independent experiments. Significant differences are indicated by asterisks. *, P

    Techniques Used: Inhibition, Expressing, Western Blot, Reverse Transcription Polymerase Chain Reaction

    Inhibition of p38 MAPK increases SGC7901/VCR to chemotherapy . SGC7901/VCR cells were treated with indicated concentrations of cisplatin, 5-FU or epirubicin, with or without SB202190 (10 μM), for 24 hours. (A) The morphology of cells was observed, and photographs were taken under the microscope. (B) Flow cytometry analysis was performed after staining with Annexin V/PI. Compared with the control cells (without SB202190), there were significantly more apoptotic cells in the SB230920 treatment group. A representative example of an experiment that was repeated three times is shown.
    Figure Legend Snippet: Inhibition of p38 MAPK increases SGC7901/VCR to chemotherapy . SGC7901/VCR cells were treated with indicated concentrations of cisplatin, 5-FU or epirubicin, with or without SB202190 (10 μM), for 24 hours. (A) The morphology of cells was observed, and photographs were taken under the microscope. (B) Flow cytometry analysis was performed after staining with Annexin V/PI. Compared with the control cells (without SB202190), there were significantly more apoptotic cells in the SB230920 treatment group. A representative example of an experiment that was repeated three times is shown.

    Techniques Used: Inhibition, Microscopy, Flow Cytometry, Cytometry, Staining

    10) Product Images from "Intracellular pathways triggered by the selective FLT-1-agonist placental growth factor in vascular smooth muscle cells exposed to hypoxia"

    Article Title: Intracellular pathways triggered by the selective FLT-1-agonist placental growth factor in vascular smooth muscle cells exposed to hypoxia

    Journal:

    doi: 10.1038/sj.bjp.0706347

    (a) Effect of AG490, SB202190 and LY294002 on the P1GF-induced proliferation of cultured VSMCs. Growth-arrested and hypoxia-treated VSMCs were stimulated with 20 ng ml −1 P1GF in the presence and in the absence (control) of the
    Figure Legend Snippet: (a) Effect of AG490, SB202190 and LY294002 on the P1GF-induced proliferation of cultured VSMCs. Growth-arrested and hypoxia-treated VSMCs were stimulated with 20 ng ml −1 P1GF in the presence and in the absence (control) of the

    Techniques Used: Cell Culture

    Effect of SB202190 (10–1000 n M ) on the contractile response induced by P1GF in preparations exposed to hypoxia. Data are expressed as percent of P1GF-induced contraction (control). Means±s.e.m. of four preparations from four animals
    Figure Legend Snippet: Effect of SB202190 (10–1000 n M ) on the contractile response induced by P1GF in preparations exposed to hypoxia. Data are expressed as percent of P1GF-induced contraction (control). Means±s.e.m. of four preparations from four animals

    Techniques Used:

    11) Product Images from "Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190"

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190

    Journal: American Journal of Physiology - Cell Physiology

    doi: 10.1152/ajpcell.00184.2015

    IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.
    Figure Legend Snippet: IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.

    Techniques Used: Incubation, Immunocytochemistry, Staining, Live Cell Imaging

    SB202190
    Figure Legend Snippet: SB202190

    Techniques Used:

    Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.
    Figure Legend Snippet: Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.

    Techniques Used: Expressing, Incubation

    12) Product Images from "Signaling Through Purinergic Receptor P2Y2 Enhances Macrophage IL-1β Production"

    Article Title: Signaling Through Purinergic Receptor P2Y2 Enhances Macrophage IL-1β Production

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms21134686

    Nucleotides induce an increase in MAPK JNK activity to enhance IL-1β production. ( A ) IL-1β ELISA in supernatants from resting peritoneal macrophages (RPMs) pretreated with BAPTA-AM at 13 μM or the PLC inhibitor U73122 at 2.5 μM for 20 min prior LPS priming with (blue bars) or without (white bars) NTPs (20 μM UTP/ATP) and then NLRP3 was activated with nigericin. A representative experiment of five is shown with +SD. ( B ) Expression by qPCR analysis of Il1b and Il6 genes from mRNA extracted from RPMs preincubated or not with U73122 at 5 μM for 20 min and then primed with LPS with or without NTPs (20 μM UTP/ATP) for 2 h. Graph shows one experiment of two represented as relative gene expression normalized to Hprt1 expression +SD. ( C ) IL-1β ELISA from peritoneal macrophages (RPMs) supernatants pretreated or not with the indicated JNK, ERK1/2, or p38 (SP600125, U0126, or SB202190 respectively) inhibitor for 20 min prior LPS priming with (blue bars) or without (white bars) nucleotides (NTPs: 20 μM UTP/ATP) for 3 h following NLRP3 activation with 3 mM ATP. One representative experiment out of 3 is shown +SD. ( D ) Extracellular LDH as a marker of cell death from RPMs treated with SP600125, U0126 or SB202190, in the presence or absence of NTPs. Average of four (SP600125) or two (U0126, SB202190) experiments +SEM is shown. ( E ) Lysates from RPMs pretreated with AR-C118925xx inhibitor and stimulated for 25 min with LPS with NTPs (20 μM UTP/ATP) were analyzed for MAPK levels by western blot (top). Dashed line indicates lanes were eliminated from the image to compose the final picture. One experiment out of 3 is shown. Quantification of band intensity of four experiments +SEM of phospho-JNK p-54 and p-46 normalized to total JNK is shown (bottom). ( F ) RPMs cell lysates from wild-type or P2ry2 −/− mice were analyzed by western blot for the indicated proteins; one experiment out of 2 is shown. ( G ) Lysates from RPMs pretreated with or without AR-C118925xx or SP600125 inhibitor for 20 min and then stimulated for 25 min with LPS or LPS+NTPs (20 μM UTP/ATP) were analyzed for JNK protein levels by western blot. ( H ) Lysates from RPMs pretreated with or without SP600125 inhibitor for 20 min and then stimulated for 2 h with LPS or LPS+NTPs (20 μM UTP/ATP) were analyzed for pro-IL-1β and β-actin protein levels by western blot. * = p
    Figure Legend Snippet: Nucleotides induce an increase in MAPK JNK activity to enhance IL-1β production. ( A ) IL-1β ELISA in supernatants from resting peritoneal macrophages (RPMs) pretreated with BAPTA-AM at 13 μM or the PLC inhibitor U73122 at 2.5 μM for 20 min prior LPS priming with (blue bars) or without (white bars) NTPs (20 μM UTP/ATP) and then NLRP3 was activated with nigericin. A representative experiment of five is shown with +SD. ( B ) Expression by qPCR analysis of Il1b and Il6 genes from mRNA extracted from RPMs preincubated or not with U73122 at 5 μM for 20 min and then primed with LPS with or without NTPs (20 μM UTP/ATP) for 2 h. Graph shows one experiment of two represented as relative gene expression normalized to Hprt1 expression +SD. ( C ) IL-1β ELISA from peritoneal macrophages (RPMs) supernatants pretreated or not with the indicated JNK, ERK1/2, or p38 (SP600125, U0126, or SB202190 respectively) inhibitor for 20 min prior LPS priming with (blue bars) or without (white bars) nucleotides (NTPs: 20 μM UTP/ATP) for 3 h following NLRP3 activation with 3 mM ATP. One representative experiment out of 3 is shown +SD. ( D ) Extracellular LDH as a marker of cell death from RPMs treated with SP600125, U0126 or SB202190, in the presence or absence of NTPs. Average of four (SP600125) or two (U0126, SB202190) experiments +SEM is shown. ( E ) Lysates from RPMs pretreated with AR-C118925xx inhibitor and stimulated for 25 min with LPS with NTPs (20 μM UTP/ATP) were analyzed for MAPK levels by western blot (top). Dashed line indicates lanes were eliminated from the image to compose the final picture. One experiment out of 3 is shown. Quantification of band intensity of four experiments +SEM of phospho-JNK p-54 and p-46 normalized to total JNK is shown (bottom). ( F ) RPMs cell lysates from wild-type or P2ry2 −/− mice were analyzed by western blot for the indicated proteins; one experiment out of 2 is shown. ( G ) Lysates from RPMs pretreated with or without AR-C118925xx or SP600125 inhibitor for 20 min and then stimulated for 25 min with LPS or LPS+NTPs (20 μM UTP/ATP) were analyzed for JNK protein levels by western blot. ( H ) Lysates from RPMs pretreated with or without SP600125 inhibitor for 20 min and then stimulated for 2 h with LPS or LPS+NTPs (20 μM UTP/ATP) were analyzed for pro-IL-1β and β-actin protein levels by western blot. * = p

    Techniques Used: Activity Assay, Enzyme-linked Immunosorbent Assay, Planar Chromatography, Expressing, Real-time Polymerase Chain Reaction, Activation Assay, Marker, Western Blot, Mouse Assay

    13) Product Images from "Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190"

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190

    Journal: American Journal of Physiology - Cell Physiology

    doi: 10.1152/ajpcell.00184.2015

    IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.
    Figure Legend Snippet: IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.

    Techniques Used: Incubation, Immunocytochemistry, Staining, Live Cell Imaging

    SB202190
    Figure Legend Snippet: SB202190

    Techniques Used:

    Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.
    Figure Legend Snippet: Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.

    Techniques Used: Expressing, Incubation

    14) Product Images from "TGF?-mediated suppression of CD248 in non-cancer cells via canonical Smad-dependent signaling pathways is uncoupled in cancer cells"

    Article Title: TGF?-mediated suppression of CD248 in non-cancer cells via canonical Smad-dependent signaling pathways is uncoupled in cancer cells

    Journal: BMC Cancer

    doi: 10.1186/1471-2407-14-113

    TGFβ-mediated suppression of CD248 via ALK5 is specific. (A, B) MEF were incubated with TGFβ (3 ng/ml) for 48 hrs in the presence or absence of the inhibitor of phosphorylated ERK1/2, U0126 10 μM (A) or phosphorylated p38, SB202190 10 μM (B) . Representative Western blots from 3 independent experiments are shown and were used to assess the effect on CD248 expression. TGFβ-coupling to either ERK1/2 or to p38 is not involved in its suppressive effects on CD248.
    Figure Legend Snippet: TGFβ-mediated suppression of CD248 via ALK5 is specific. (A, B) MEF were incubated with TGFβ (3 ng/ml) for 48 hrs in the presence or absence of the inhibitor of phosphorylated ERK1/2, U0126 10 μM (A) or phosphorylated p38, SB202190 10 μM (B) . Representative Western blots from 3 independent experiments are shown and were used to assess the effect on CD248 expression. TGFβ-coupling to either ERK1/2 or to p38 is not involved in its suppressive effects on CD248.

    Techniques Used: Incubation, Western Blot, Expressing

    15) Product Images from "GSK3 is a negative regulator of the thermogenic program in brown adipocytes"

    Article Title: GSK3 is a negative regulator of the thermogenic program in brown adipocytes

    Journal: Scientific Reports

    doi: 10.1038/s41598-018-21795-y

    Inhibition of GSK3 promotes activation of the MKK3/6-p38 MAPK-ATF2 signaling module. ( a ) Immunoblot analysis for activating phosphorylations of proteins of the MKK3/6-p38 MAPK-ATF2 signaling module in primary brown adipocytes pre-treated with 10 μM SB216763 for 1 h before stimulation with 0.1 μM ISO for 1 h. ( b ) Immunoblot analysis of total and phosphorylated p38 MAPK in immortalized brown adipocytes overexpressing GSK3β mutants or empty vector. Cells were treated with 0.1 μM ISO for 1 h. ( c ) Fgf21 expression in primary brown adipocytes pre-treated with 10 μM SB202190 (p38 MAPK inhibitor) for 1 h before treatment with 10 μM SB216763 (GSK3 inhibitor) for 1 h, followed by stimulation with 0.1 μM ISO for additional 6 h. ( d ) Schematic presentation of the proposed mechanism through which GSK3 regulates the thermogenic gene program in brown adipocytes. Data presented as mean of means +SEM (n = 3). Statistical significance was determined by two-way ANOVA with repeated measures and Tukey’s post hoc test for multiple comparisons. *p
    Figure Legend Snippet: Inhibition of GSK3 promotes activation of the MKK3/6-p38 MAPK-ATF2 signaling module. ( a ) Immunoblot analysis for activating phosphorylations of proteins of the MKK3/6-p38 MAPK-ATF2 signaling module in primary brown adipocytes pre-treated with 10 μM SB216763 for 1 h before stimulation with 0.1 μM ISO for 1 h. ( b ) Immunoblot analysis of total and phosphorylated p38 MAPK in immortalized brown adipocytes overexpressing GSK3β mutants or empty vector. Cells were treated with 0.1 μM ISO for 1 h. ( c ) Fgf21 expression in primary brown adipocytes pre-treated with 10 μM SB202190 (p38 MAPK inhibitor) for 1 h before treatment with 10 μM SB216763 (GSK3 inhibitor) for 1 h, followed by stimulation with 0.1 μM ISO for additional 6 h. ( d ) Schematic presentation of the proposed mechanism through which GSK3 regulates the thermogenic gene program in brown adipocytes. Data presented as mean of means +SEM (n = 3). Statistical significance was determined by two-way ANOVA with repeated measures and Tukey’s post hoc test for multiple comparisons. *p

    Techniques Used: Inhibition, Activation Assay, Plasmid Preparation, Expressing

    16) Product Images from "Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190"

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190

    Journal: American Journal of Physiology - Cell Physiology

    doi: 10.1152/ajpcell.00184.2015

    IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.
    Figure Legend Snippet: IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.

    Techniques Used: Incubation, Immunocytochemistry, Staining, Live Cell Imaging

    SB202190
    Figure Legend Snippet: SB202190

    Techniques Used:

    Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.
    Figure Legend Snippet: Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.

    Techniques Used: Expressing, Incubation

    17) Product Images from "Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190"

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190

    Journal: American Journal of Physiology - Cell Physiology

    doi: 10.1152/ajpcell.00184.2015

    IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.
    Figure Legend Snippet: IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.

    Techniques Used: Incubation, Immunocytochemistry, Staining, Live Cell Imaging

    SB202190
    Figure Legend Snippet: SB202190

    Techniques Used:

    Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.
    Figure Legend Snippet: Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.

    Techniques Used: Expressing, Incubation

    18) Product Images from "Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190"

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190

    Journal: American Journal of Physiology - Cell Physiology

    doi: 10.1152/ajpcell.00184.2015

    IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.
    Figure Legend Snippet: IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.

    Techniques Used: Incubation, Immunocytochemistry, Staining, Live Cell Imaging

    SB202190
    Figure Legend Snippet: SB202190

    Techniques Used:

    Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.
    Figure Legend Snippet: Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.

    Techniques Used: Expressing, Incubation

    19) Product Images from "Trichoplein binds PCM1 and controls endothelial cell function by regulating autophagy"

    Article Title: Trichoplein binds PCM1 and controls endothelial cell function by regulating autophagy

    Journal: EMBO Reports

    doi: 10.15252/embr.201948192

    Identification of the mechanism of p62 accumulation Representative images for p62 of control and TCHP knock‐down HUVECs treated with BAY11‐7082 (300 nM) or TYRPHOSTIN AG1288 (300 nM) or SB202190 (300 nM) or vehicle (DMSO) for 48 h. Scale bars, 50 μm. (B) Expression of IL‐6, IL‐8 and IL‐1β (one‐way ANOVA; IL‐8: ** P = 0.008 vs. control DMSO; # P = 0.0198 (BAY) # P = 0.01 (AG) vs. shTCHP DMSO; IL‐6: ** P = 0.0023 vs. control DMSO; # P = 0.0063 (BAY) # P = 0.0108 (AG) vs. shTCHP DMSO; IL‐1β: ** P = 0.0011 vs. control DMSO; # P = 0.0004 (BAY) # P = 0.0015 (AG) vs. shTCHP DMSO) and (C), migration speed was measured (one‐way ANOVA; ** P = 0.0003 vs. control DMSO; # P = 0.0451 vs. shTCHP DMSO). Western blot analysis for anti‐phosphor‐NF‐κB (S536), total NF‐κB, in TCHP knock‐down and control cells treated with BAY or vehicle. Below panel: quantification (one‐way ANOVA; ** P = 0.0014 vs. control DMSO; # P = 0.0293 vs. shTCHP DMSO). p62 expression in TCHP knock‐down and control cells treated with BAY or vehicle (one‐way ANOVA; ** P = 0.0004 vs. control DMSO; # P = 0.0243 vs. shTCHP DMSO). p62 expression in TCHP knock‐down and control cells treated with siRELA or control (one‐way ANOVA; ** P = 0.0023 vs. control siRNA; # P = 0.0127 vs. shTCHP siRELA). ChIP‐qPCR analysis confirms the of NF‐κB p65 enrichment to IκBα and p62 promoter in TCHP knock‐down cells (unpaired t ‐test; ** P = 0.0057 and ** P = 0.0037 vs. control, respectively). Data information: Statistical analyses were performed on at least three independent experiments. Data are represented as mean ± SD.
    Figure Legend Snippet: Identification of the mechanism of p62 accumulation Representative images for p62 of control and TCHP knock‐down HUVECs treated with BAY11‐7082 (300 nM) or TYRPHOSTIN AG1288 (300 nM) or SB202190 (300 nM) or vehicle (DMSO) for 48 h. Scale bars, 50 μm. (B) Expression of IL‐6, IL‐8 and IL‐1β (one‐way ANOVA; IL‐8: ** P = 0.008 vs. control DMSO; # P = 0.0198 (BAY) # P = 0.01 (AG) vs. shTCHP DMSO; IL‐6: ** P = 0.0023 vs. control DMSO; # P = 0.0063 (BAY) # P = 0.0108 (AG) vs. shTCHP DMSO; IL‐1β: ** P = 0.0011 vs. control DMSO; # P = 0.0004 (BAY) # P = 0.0015 (AG) vs. shTCHP DMSO) and (C), migration speed was measured (one‐way ANOVA; ** P = 0.0003 vs. control DMSO; # P = 0.0451 vs. shTCHP DMSO). Western blot analysis for anti‐phosphor‐NF‐κB (S536), total NF‐κB, in TCHP knock‐down and control cells treated with BAY or vehicle. Below panel: quantification (one‐way ANOVA; ** P = 0.0014 vs. control DMSO; # P = 0.0293 vs. shTCHP DMSO). p62 expression in TCHP knock‐down and control cells treated with BAY or vehicle (one‐way ANOVA; ** P = 0.0004 vs. control DMSO; # P = 0.0243 vs. shTCHP DMSO). p62 expression in TCHP knock‐down and control cells treated with siRELA or control (one‐way ANOVA; ** P = 0.0023 vs. control siRNA; # P = 0.0127 vs. shTCHP siRELA). ChIP‐qPCR analysis confirms the of NF‐κB p65 enrichment to IκBα and p62 promoter in TCHP knock‐down cells (unpaired t ‐test; ** P = 0.0057 and ** P = 0.0037 vs. control, respectively). Data information: Statistical analyses were performed on at least three independent experiments. Data are represented as mean ± SD.

    Techniques Used: Expressing, Migration, Western Blot, Chromatin Immunoprecipitation, Real-time Polymerase Chain Reaction

    20) Product Images from "Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190"

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190

    Journal: American Journal of Physiology - Cell Physiology

    doi: 10.1152/ajpcell.00184.2015

    IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.
    Figure Legend Snippet: IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.

    Techniques Used: Incubation, Immunocytochemistry, Staining, Live Cell Imaging

    SB202190
    Figure Legend Snippet: SB202190

    Techniques Used:

    Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.
    Figure Legend Snippet: Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.

    Techniques Used: Expressing, Incubation

    21) Product Images from "Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190"

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190

    Journal: American Journal of Physiology - Cell Physiology

    doi: 10.1152/ajpcell.00184.2015

    IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.
    Figure Legend Snippet: IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.

    Techniques Used: Incubation, Immunocytochemistry, Staining, Live Cell Imaging

    SB202190
    Figure Legend Snippet: SB202190

    Techniques Used:

    Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.
    Figure Legend Snippet: Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.

    Techniques Used: Expressing, Incubation

    22) Product Images from "Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190"

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190

    Journal: American Journal of Physiology - Cell Physiology

    doi: 10.1152/ajpcell.00184.2015

    IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.
    Figure Legend Snippet: IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.

    Techniques Used: Incubation, Immunocytochemistry, Staining, Live Cell Imaging

    SB202190
    Figure Legend Snippet: SB202190

    Techniques Used:

    Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.
    Figure Legend Snippet: Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.

    Techniques Used: Expressing, Incubation

    23) Product Images from "TNF‐α signaling regulates RUNX1 function in endothelial cells, et al. TNF‐α signaling regulates RUNX1 function in endothelial cells"

    Article Title: TNF‐α signaling regulates RUNX1 function in endothelial cells, et al. TNF‐α signaling regulates RUNX1 function in endothelial cells

    Journal: The FASEB Journal

    doi: 10.1096/fj.202001668R

    RUNX1 expression was reduced by blocking the TNF‐α mediated JNK signaling pathway. Treatment of HRMECs with TNF‐α (5 ng/mL) in combination with TNFR1 inhibitor, CAY10500 (1 μM); NF‐κB inhibitors, CAPE (1 μM) and Honokiol (5 μM); dual NF‐κB and JNK inhibitor, Withaferin A (5 μM); JNK inhibitors, SP600125 (1 μM) and TCS JNK 6o (5 μM) and p38/MAPK inhibitors, SB239063 (5 μM) and SB202190 (5 μM). Cells were treated for (A) 48 hours for quantification by qRT‐PCR (n = 6) and (B) 72 hours for Western blot analyses (n = 2). qRT‐PCR data are shown as (log 2 ‐(fold change)), normalized to endogenous HPRT expression and unstimulated control. Western blot analyses are normalized to β‐actin and unstimulated control. Shown are mean values + SEM. Data are analyzed using one‐way ANOVA with Dunnett's post hoc test. * P
    Figure Legend Snippet: RUNX1 expression was reduced by blocking the TNF‐α mediated JNK signaling pathway. Treatment of HRMECs with TNF‐α (5 ng/mL) in combination with TNFR1 inhibitor, CAY10500 (1 μM); NF‐κB inhibitors, CAPE (1 μM) and Honokiol (5 μM); dual NF‐κB and JNK inhibitor, Withaferin A (5 μM); JNK inhibitors, SP600125 (1 μM) and TCS JNK 6o (5 μM) and p38/MAPK inhibitors, SB239063 (5 μM) and SB202190 (5 μM). Cells were treated for (A) 48 hours for quantification by qRT‐PCR (n = 6) and (B) 72 hours for Western blot analyses (n = 2). qRT‐PCR data are shown as (log 2 ‐(fold change)), normalized to endogenous HPRT expression and unstimulated control. Western blot analyses are normalized to β‐actin and unstimulated control. Shown are mean values + SEM. Data are analyzed using one‐way ANOVA with Dunnett's post hoc test. * P

    Techniques Used: Expressing, Blocking Assay, Quantitative RT-PCR, Western Blot

    24) Product Images from "Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190"

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190

    Journal: American Journal of Physiology - Cell Physiology

    doi: 10.1152/ajpcell.00184.2015

    IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.
    Figure Legend Snippet: IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.

    Techniques Used: Incubation, Immunocytochemistry, Staining, Live Cell Imaging

    SB202190
    Figure Legend Snippet: SB202190

    Techniques Used:

    Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.
    Figure Legend Snippet: Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.

    Techniques Used: Expressing, Incubation

    Related Articles

    Activation Assay:

    Article Title: Direct activation of the mitochondrial calcium uniporter by natural plant flavonoids
    Article Snippet: However, the maximum effect was not completely reached, even at a concentration of 40 μM which stimulated mitochondrial Ca2+ uptake by 19±1-fold (mean±S.E.M., n =4) over the control values. .. The large magnitude of this activation is consistent with that previously shown for SB202190, suggesting that both kinds of compounds acted by the same mechanism. ..

    Mass Spectrometry:

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190
    Article Snippet: Except for α3 -integrin, which was transiently increased, we detected no changes in abundance of these latter mRNAs when comparing cells incubated with and without SB202190 for up to 30 h ( ). .. To more broadly analyze changes in protein abundance, we performed quantitative mass spectroscopy on paired protein lysates at three intervals following 48 h of incubation in DM with SB202190 and IGF-I: 4, 12, and 24 after maintenance or removal of SB202190. .. We also collected protein lysates from cells incubated in DM plus IGF-I for 48 h. From these lysates, we identified 2,690 proteins whose levels could be tracked at different time points.

    Incubation:

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190
    Article Snippet: Except for α3 -integrin, which was transiently increased, we detected no changes in abundance of these latter mRNAs when comparing cells incubated with and without SB202190 for up to 30 h ( ). .. To more broadly analyze changes in protein abundance, we performed quantitative mass spectroscopy on paired protein lysates at three intervals following 48 h of incubation in DM with SB202190 and IGF-I: 4, 12, and 24 after maintenance or removal of SB202190. .. We also collected protein lysates from cells incubated in DM plus IGF-I for 48 h. From these lysates, we identified 2,690 proteins whose levels could be tracked at different time points.

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190
    Article Snippet: For subsequent analysis, summed protein intensity values of < 10,000 obtained from lysates of cells incubated in DM with SB202190 and IGF-I for 48 h were eliminated from further consideration. .. Results for the remaining 2,690 proteins were normalized by determination of the ratio of protein intensity at different time points and treatments to protein intensity from lysates of cells incubated for 48 h in DM with SB202190 and IGF-I. .. For , A and B , the following ratios were analyzed: 1 ) cells incubated in DM and IGF-I for 24 h after removal of SB202190 vs. cells exposed to SB202190 plus IGF-I for 48 h, 2 ) cells incubated in DM and IGF-I for 24 h after removal of SB202190 vs. cells in DM plus SB202190 and IGF-I for all 72 h, and 3 ) cells in DM and IGF-I for 48 h vs. cells in DM plus SB202190 and IGF-I for 48 h (for a complete list of identified proteins, raw summed reporter ion intensities, and normalized data used to calculate protein abundance ratios, see Supplemental Table S1 in Supplemental Material for this article available online at the Journal website).

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190
    Article Snippet: We also measured several other mRNAs encoding fusion-associated proteins that were not found consistently in our mass spectrometry data (see below), including α3 -integrin, M-cadherin, myomaker (Tmemb8C) , Brag2, Dock5, and Fak1 ( ). .. Except for α3 -integrin, which was transiently increased, we detected no changes in abundance of these latter mRNAs when comparing cells incubated with and without SB202190 for up to 30 h ( ). .. To more broadly analyze changes in protein abundance, we performed quantitative mass spectroscopy on paired protein lysates at three intervals following 48 h of incubation in DM with SB202190 and IGF-I: 4, 12, and 24 after maintenance or removal of SB202190.

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190
    Article Snippet: .. We next examined protein expression in C2 muscle cells after SB202190 was maintained in the medium or removed from the medium, beginning at 44 h after onset of incubation in DM. .. There was little alteration in levels of muscle transcription factors, MyoD, myogenin, and Mef2C during the subsequent 30 h, although an increase was noted in muscle structural proteins, troponin-T and myosin heavy chain, beginning at 8–12 h after removal of SB202190 ( ).

    Polymerase Chain Reaction:

    Article Title: TNF‐α signaling regulates RUNX1 function in endothelial cells, et al. TNF‐α signaling regulates RUNX1 function in endothelial cells
    Article Snippet: To confirm our hypothesis that TNF‐α is binding and signaling through TNFR1, we used a TNF‐α‐TNFR1 binding inhibitor, CAY10500, as a positive control. .. We then used PCR (Figure ) and Western blot (Figure ) analyses to measure RUNX1 expression levels when HRMECs were co‐treated with TNF‐α and a selective inhibitor [Caffeic acid phenethyl ester (CAPE) and Honokiol, NF‐κB inhibitors; Withaferin A, a dual NF‐κB/JNK inhibitor; SP600125 and TCS JNK 6o, JNK inhibitors; SB239063 and SB202190, p38/MAPK inhibitors]. .. Only the dual NF‐κB/JNK inhibitor Withaferin A, and the JNK inhibitors SP600125 and TCS JNK 6o efficiently blocked the up‐regulation of RUNX1 expression by TNF‐α.

    Western Blot:

    Article Title: TNF‐α signaling regulates RUNX1 function in endothelial cells, et al. TNF‐α signaling regulates RUNX1 function in endothelial cells
    Article Snippet: To confirm our hypothesis that TNF‐α is binding and signaling through TNFR1, we used a TNF‐α‐TNFR1 binding inhibitor, CAY10500, as a positive control. .. We then used PCR (Figure ) and Western blot (Figure ) analyses to measure RUNX1 expression levels when HRMECs were co‐treated with TNF‐α and a selective inhibitor [Caffeic acid phenethyl ester (CAPE) and Honokiol, NF‐κB inhibitors; Withaferin A, a dual NF‐κB/JNK inhibitor; SP600125 and TCS JNK 6o, JNK inhibitors; SB239063 and SB202190, p38/MAPK inhibitors]. .. Only the dual NF‐κB/JNK inhibitor Withaferin A, and the JNK inhibitors SP600125 and TCS JNK 6o efficiently blocked the up‐regulation of RUNX1 expression by TNF‐α.

    Expressing:

    Article Title: TNF‐α signaling regulates RUNX1 function in endothelial cells, et al. TNF‐α signaling regulates RUNX1 function in endothelial cells
    Article Snippet: To confirm our hypothesis that TNF‐α is binding and signaling through TNFR1, we used a TNF‐α‐TNFR1 binding inhibitor, CAY10500, as a positive control. .. We then used PCR (Figure ) and Western blot (Figure ) analyses to measure RUNX1 expression levels when HRMECs were co‐treated with TNF‐α and a selective inhibitor [Caffeic acid phenethyl ester (CAPE) and Honokiol, NF‐κB inhibitors; Withaferin A, a dual NF‐κB/JNK inhibitor; SP600125 and TCS JNK 6o, JNK inhibitors; SB239063 and SB202190, p38/MAPK inhibitors]. .. Only the dual NF‐κB/JNK inhibitor Withaferin A, and the JNK inhibitors SP600125 and TCS JNK 6o efficiently blocked the up‐regulation of RUNX1 expression by TNF‐α.

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190
    Article Snippet: .. We next examined protein expression in C2 muscle cells after SB202190 was maintained in the medium or removed from the medium, beginning at 44 h after onset of incubation in DM. .. There was little alteration in levels of muscle transcription factors, MyoD, myogenin, and Mef2C during the subsequent 30 h, although an increase was noted in muscle structural proteins, troponin-T and myosin heavy chain, beginning at 8–12 h after removal of SB202190 ( ).

    other:

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190
    Article Snippet: Muscle differentiation was induced when co-cultured cells reached ∼95% of confluent density by replacement of growth medium with differentiation medium (DM: DMEM + 2% horse serum) ± SB202190 (5 μM) ± R3-IGF-I (1 nM).

    Concentration Assay:

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190
    Article Snippet: .. SB202190 (Tocris Bioscience, Bristol, UK) was solubilized in DMSO and stored at 1,000× final concentration in aliquots at −80°C; it was diluted into medium immediately prior to use. .. Primary antibodies were purchased as follows: anti-myogenin (product no. F5D from W. E. Wright), anti-myosin heavy chain (product no. MF20 from D. A. Fischman), and anti-troponin-T (product no. CT3 from J. J.-C. Lin) from Developmental Studies Hybridoma Bank (Iowa City, IA); anti-Mef2c (catalog no. IA-14) from Covance (Madison, WI); anti-MyoD (catalog no. 5.8A) from BD-Pharmingen (San Jose, CA); anti-Akt (catalog no. 4691), anti-phosphorylated (p) AktThr308 (catalog no. 2965), anti-p38 (catalog no. 8690), anti-p-p38 (catalog no. 4511), anti-Erk (catalog no. 4695), anti-p-Erk (catalog no. 4370), anti-mammalian target of rapamycin (mTor; catalog no. 2983), and anti-p-mTor (catalog no. 5536) from Cell Signaling (Beverly, MA); and anti-α-tubulin (catalog no. B-5-1-2) from Sigma-Aldrich.

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    Tocris sb202190
    IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor <t>SB202190.</t> A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.
    Sb202190, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190

    doi: 10.1152/ajpcell.00184.2015

    Figure Lengend Snippet: IGF-I promotes muscle differentiation, but not myocyte fusion, in the presence of the p38 inhibitor SB202190. A : experimental plan. Confluent C2 myoblasts were incubated in DM with SB202190 (5 μM) ± R3-IGF-I (1 nM). After 44 h, medium was replaced, and new DM was added ± SB202190 for an additional 30 h. B : immunocytochemistry for troponin-T (red) and myogenin (green). Magnification ×100 (scale bars = 100 μm). C : immunocytochemistry for troponin-T (red) and myogenin (green) and staining for nuclei with Hoechst 33258 (blue). Magnification ×200 (scale bars = 50 μm). D : changes in the extent of myocyte fusion over time during incubation ± SB during live-cell imaging.

    Article Snippet: SB202190 (Tocris Bioscience, Bristol, UK) was solubilized in DMSO and stored at 1,000× final concentration in aliquots at −80°C; it was diluted into medium immediately prior to use.

    Techniques: Incubation, Immunocytochemistry, Staining, Live Cell Imaging

    SB202190

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190

    doi: 10.1152/ajpcell.00184.2015

    Figure Lengend Snippet: SB202190

    Article Snippet: SB202190 (Tocris Bioscience, Bristol, UK) was solubilized in DMSO and stored at 1,000× final concentration in aliquots at −80°C; it was diluted into medium immediately prior to use.

    Techniques:

    Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190

    doi: 10.1152/ajpcell.00184.2015

    Figure Lengend Snippet: Muscle and signaling protein expression after removal of the p38 inhibitor SB202190. Protein expression by immunoblotting for MyoD, myogenin, Mef2C, troponin-T, myosin heavy chain (MHC), phosphorylated (p)-p38 and total p38, p-Erk and total Erk, p-Akt (pAkt S308 ) and total Akt, p-mammalian target of rapamycin (mTor) and total mTor, and α-tubulin by immunoblotting during incubation of C2 myoblasts in DM plus SB202190 and R3-IGF-I or after removal of SB202190. Molecular mass markers are indicated at right . Images are representative of ≥3 independent experiments.

    Article Snippet: SB202190 (Tocris Bioscience, Bristol, UK) was solubilized in DMSO and stored at 1,000× final concentration in aliquots at −80°C; it was diluted into medium immediately prior to use.

    Techniques: Expressing, Incubation

    RUNX1 expression was reduced by blocking the TNF‐α mediated JNK signaling pathway. Treatment of HRMECs with TNF‐α (5 ng/mL) in combination with TNFR1 inhibitor, CAY10500 (1 μM); NF‐κB inhibitors, CAPE (1 μM) and Honokiol (5 μM); dual NF‐κB and JNK inhibitor, Withaferin A (5 μM); JNK inhibitors, SP600125 (1 μM) and TCS JNK 6o (5 μM) and p38/MAPK inhibitors, SB239063 (5 μM) and SB202190 (5 μM). Cells were treated for (A) 48 hours for quantification by qRT‐PCR (n = 6) and (B) 72 hours for Western blot analyses (n = 2). qRT‐PCR data are shown as (log 2 ‐(fold change)), normalized to endogenous HPRT expression and unstimulated control. Western blot analyses are normalized to β‐actin and unstimulated control. Shown are mean values + SEM. Data are analyzed using one‐way ANOVA with Dunnett's post hoc test. * P

    Journal: The FASEB Journal

    Article Title: TNF‐α signaling regulates RUNX1 function in endothelial cells, et al. TNF‐α signaling regulates RUNX1 function in endothelial cells

    doi: 10.1096/fj.202001668R

    Figure Lengend Snippet: RUNX1 expression was reduced by blocking the TNF‐α mediated JNK signaling pathway. Treatment of HRMECs with TNF‐α (5 ng/mL) in combination with TNFR1 inhibitor, CAY10500 (1 μM); NF‐κB inhibitors, CAPE (1 μM) and Honokiol (5 μM); dual NF‐κB and JNK inhibitor, Withaferin A (5 μM); JNK inhibitors, SP600125 (1 μM) and TCS JNK 6o (5 μM) and p38/MAPK inhibitors, SB239063 (5 μM) and SB202190 (5 μM). Cells were treated for (A) 48 hours for quantification by qRT‐PCR (n = 6) and (B) 72 hours for Western blot analyses (n = 2). qRT‐PCR data are shown as (log 2 ‐(fold change)), normalized to endogenous HPRT expression and unstimulated control. Western blot analyses are normalized to β‐actin and unstimulated control. Shown are mean values + SEM. Data are analyzed using one‐way ANOVA with Dunnett's post hoc test. * P

    Article Snippet: We then used PCR (Figure ) and Western blot (Figure ) analyses to measure RUNX1 expression levels when HRMECs were co‐treated with TNF‐α and a selective inhibitor [Caffeic acid phenethyl ester (CAPE) and Honokiol, NF‐κB inhibitors; Withaferin A, a dual NF‐κB/JNK inhibitor; SP600125 and TCS JNK 6o, JNK inhibitors; SB239063 and SB202190, p38/MAPK inhibitors].

    Techniques: Expressing, Blocking Assay, Quantitative RT-PCR, Western Blot