p38 inhibitor sb202190 Millipore Search Results


  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 95
    Millipore p38 mapk
    Proposed model. When endometrial cancer cells are exposed to acidic medium the <t>p38</t> <t>MAPK</t> signaling pathway is activated and an increase in SR proteins phosphorylation that will eventually regulate the VEGF alternative splicing takes place. In acidosis, not only VEGF expression is increased but also a modification of the alternative splicing occurs, where an increase in the proportion of VEGF121 versus VEGF145, 165, and 189 is observed
    P38 Mapk, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 348 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p38 mapk/product/Millipore
    Average 95 stars, based on 348 article reviews
    Price from $9.99 to $1999.99
    p38 mapk - by Bioz Stars, 2020-02
    95/100 stars
      Buy from Supplier

    79
    Millipore p38 sb202190 inhibitors
    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, <t>SB202190.</t> 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 <t>p38)</t> 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.
    P38 Sb202190 Inhibitors, supplied by Millipore, used in various techniques. Bioz Stars score: 79/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p38 sb202190 inhibitors/product/Millipore
    Average 79 stars, based on 9 article reviews
    Price from $9.99 to $1999.99
    p38 sb202190 inhibitors - by Bioz Stars, 2020-02
    79/100 stars
      Buy from Supplier

    77
    Millipore p38 inhibitor sb202109
    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, <t>SB202190.</t> 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 <t>p38)</t> 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.
    P38 Inhibitor Sb202109, supplied by Millipore, used in various techniques. Bioz Stars score: 77/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p38 inhibitor sb202109/product/Millipore
    Average 77 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    p38 inhibitor sb202109 - by Bioz Stars, 2020-02
    77/100 stars
      Buy from Supplier

    88
    Millipore m sb202190 p38 mapk inhibitor
    Effect of the <t>p38</t> <t>MAPK</t> inhibitor <t>SB202190</t> on SOD3 mRNA expression. (a–c) The inhibition of p38 MAPK phosphorylation increased the SOD3 expression in human TPC1 and 8505c cells, while SB202190 treatment did not alter the SOD3 mRNA synthesis in Nthy cells modeling normal thyroid. (d–f) The inhibitor treatment increased sod3 mRNA expression in PC Cl3-derived PC PTC1 and PC E1A cells, while the treatment had no effect on PC Cl3 control cells modeling normal thyroid. (g–j) FRLT5 cell clones V13, V21, and V39 stably transfected with RAS showed a significant increase in sod3 mRNA expression after SB202190 treatment, whereas SB202190 had no effect on FRLT5 control cells, which is consistent with the results using the other cell models. (k, m) The Western blot analysis for p38 MAPK activation in FRLT5 control cells, clone V13, clone V21, and clone V39. The histogram (panel (m)) suggested significantly increased p38 MAPK phosphorylation in FRLT5-derived clones compared to control cells. Total p38 MAPK was used to normalize the phosphorylation level. (l, n) The transient transfection of an H-RasV12 expression plasmid into HEK 293T cells showed a gradual increase in p38 MAPK phosphorylation that corresponded to the amount of plasmid transfected. Total p38 MAPK was used to normalize the phosphorylation level. The data are expressed as the mean ± SD. The p values are represented ( ∗ p
    M Sb202190 P38 Mapk Inhibitor, supplied by Millipore, used in various techniques. Bioz Stars score: 88/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/m sb202190 p38 mapk inhibitor/product/Millipore
    Average 88 stars, based on 7 article reviews
    Price from $9.99 to $1999.99
    m sb202190 p38 mapk inhibitor - by Bioz Stars, 2020-02
    88/100 stars
      Buy from Supplier

    78
    Millipore p38 mapk inhibitor sb202190 fhpi
    Effect of <t>p38</t> <t>MAPK</t> inhibitor <t>SB202190</t> <t>(FHPI)</t> on CAT expression from the UL4-CAT promoter in recombinant virus-infected HFFs. Confluent HFFs were serum starved for 24 h and then treated with FHPI for 1 h before infection with various recombinant viruses in the presence of FHPI in quadruplicate as described in Materials and Methods. Cells were harvested at 14 h after infection and subjected to CAT assays. The results of the CAT assays were averaged, and the standard deviations were calculated. The CAT activity per microgram of protein at various concentrations of the drug is relative to that of the nontreated recombinant viruses.
    P38 Mapk Inhibitor Sb202190 Fhpi, supplied by Millipore, used in various techniques. Bioz Stars score: 78/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p38 mapk inhibitor sb202190 fhpi/product/Millipore
    Average 78 stars, based on 5 article reviews
    Price from $9.99 to $1999.99
    p38 mapk inhibitor sb202190 fhpi - by Bioz Stars, 2020-02
    78/100 stars
      Buy from Supplier

    95
    Millipore p38 inhibitors
    Effect of KM11073 on the activation of <t>p38.</t> Cells (1 × 10 5 cells/well) were cultured in a 6-well plate for 1 day and then incubated with DMEM containing 5% FBS in the presence or absence of BMP-2 and/or KM11073 ( A ). Inhibitory effects of p38 inhibitors (1, SB202190; 2, PD169316; 3, SB203580) on the activation of p38 by BMP-2 and KM11073. Western blot analysis was performed with protein samples prepared with cells treated with each inhibitor for 30 min and then incubated with BMP-2 and KM11073 for 30 min ( B ). The relative, normalized ratio between phosphorylated protein and the protein itself was presented.
    P38 Inhibitors, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 42 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p38 inhibitors/product/Millipore
    Average 95 stars, based on 42 article reviews
    Price from $9.99 to $1999.99
    p38 inhibitors - by Bioz Stars, 2020-02
    95/100 stars
      Buy from Supplier

    79
    Millipore p38 mitogen activated protein kinase inhibitor sb202190
    Effects of non-Smad signaling on Dkk1 and Sost expression in osteoblasts. ( A ) Effects of <t>p38</t> <t>MAPK</t> inhibitor <t>SB202190</t> on Dkk1 and Sost expression using primary osteoblasts from newborn wild-type mice as assessed by qRT-PCR. mRNA was isolated from wild-type osteoblasts pretreated with SB202190 (10 µM) or DMSO in the absence of serum for 1 hour prior to the addition of BMP2 (100 ng/mL) or PBS for 3 hours. Upregulation of Dkk1 expression by BMP2 treatment was restored by SB202190 pretreatment. Sost expression was increased significantly by BMP2 treatment with SB202190 pretreatment. Values are expressed relative to untreated osteoblasts (neither SB202190 nor BMP2) (mean ± SD; t test; * p
    P38 Mitogen Activated Protein Kinase Inhibitor Sb202190, supplied by Millipore, used in various techniques. Bioz Stars score: 79/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p38 mitogen activated protein kinase inhibitor sb202190/product/Millipore
    Average 79 stars, based on 4 article reviews
    Price from $9.99 to $1999.99
    p38 mitogen activated protein kinase inhibitor sb202190 - by Bioz Stars, 2020-02
    79/100 stars
      Buy from Supplier

    77
    Millipore p38 stress activated protein kinase sapk inhibitor sb202190
    Response of hepcidin transcript levels to serum deprivation and protein kinase inhibition. ( A ) Serum withdrawal rapidly decreased hepcidin transcript levels in Huh7 cells. ( B ) After 40 h of FCS reduction from 10% to 0.4%, hepcidin transcripts were hardly detectable by RPA in HepG2 cells, whereas hypoxic IGFBP1 induction was not affected. Representative of three independent experiments. U6sn RNA served as loading control. ( C ) Exposure of Huh7 cells to protein kinase inhibitors revealed that the pan kinase inhibitor staurosporine (stauro; 0.5 µM) and the PI3 kinase inhibitor LY294002 (LY; 10 µM) reduced hepcidin expression similar to serum deprivation, whereas the <t>p38</t> SAP kinase inhibitor <t>SB202190</t> (SB; 10 µM) had no effect and the MEK1/2 inhibitor UO126 (1 µM) even increased HAMP/18S ratios. Data are results of qRT PCR analyses and given as means of three independent experiments±SEM; *p
    P38 Stress Activated Protein Kinase Sapk Inhibitor Sb202190, supplied by Millipore, used in various techniques. Bioz Stars score: 77/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p38 stress activated protein kinase sapk inhibitor sb202190/product/Millipore
    Average 77 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    p38 stress activated protein kinase sapk inhibitor sb202190 - by Bioz Stars, 2020-02
    77/100 stars
      Buy from Supplier

    87
    Millipore sr 202 sb202190
    Response of hepcidin transcript levels to serum deprivation and protein kinase inhibition. ( A ) Serum withdrawal rapidly decreased hepcidin transcript levels in Huh7 cells. ( B ) After 40 h of FCS reduction from 10% to 0.4%, hepcidin transcripts were hardly detectable by RPA in HepG2 cells, whereas hypoxic IGFBP1 induction was not affected. Representative of three independent experiments. U6sn RNA served as loading control. ( C ) Exposure of Huh7 cells to protein kinase inhibitors revealed that the pan kinase inhibitor staurosporine (stauro; 0.5 µM) and the PI3 kinase inhibitor LY294002 (LY; 10 µM) reduced hepcidin expression similar to serum deprivation, whereas the <t>p38</t> SAP kinase inhibitor <t>SB202190</t> (SB; 10 µM) had no effect and the MEK1/2 inhibitor UO126 (1 µM) even increased HAMP/18S ratios. Data are results of qRT PCR analyses and given as means of three independent experiments±SEM; *p
    Sr 202 Sb202190, supplied by Millipore, used in various techniques. Bioz Stars score: 87/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/sr 202 sb202190/product/Millipore
    Average 87 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    sr 202 sb202190 - by Bioz Stars, 2020-02
    87/100 stars
      Buy from Supplier

    95
    Millipore mitogen activated protein kinase
    Response of hepcidin transcript levels to serum deprivation and protein kinase inhibition. ( A ) Serum withdrawal rapidly decreased hepcidin transcript levels in Huh7 cells. ( B ) After 40 h of FCS reduction from 10% to 0.4%, hepcidin transcripts were hardly detectable by RPA in HepG2 cells, whereas hypoxic IGFBP1 induction was not affected. Representative of three independent experiments. U6sn RNA served as loading control. ( C ) Exposure of Huh7 cells to protein kinase inhibitors revealed that the pan kinase inhibitor staurosporine (stauro; 0.5 µM) and the PI3 kinase inhibitor LY294002 (LY; 10 µM) reduced hepcidin expression similar to serum deprivation, whereas the <t>p38</t> SAP kinase inhibitor <t>SB202190</t> (SB; 10 µM) had no effect and the MEK1/2 inhibitor UO126 (1 µM) even increased HAMP/18S ratios. Data are results of qRT PCR analyses and given as means of three independent experiments±SEM; *p
    Mitogen Activated Protein Kinase, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 85 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mitogen activated protein kinase/product/Millipore
    Average 95 stars, based on 85 article reviews
    Price from $9.99 to $1999.99
    mitogen activated protein kinase - by Bioz Stars, 2020-02
    95/100 stars
      Buy from Supplier

    Image Search Results


    Proposed model. When endometrial cancer cells are exposed to acidic medium the p38 MAPK signaling pathway is activated and an increase in SR proteins phosphorylation that will eventually regulate the VEGF alternative splicing takes place. In acidosis, not only VEGF expression is increased but also a modification of the alternative splicing occurs, where an increase in the proportion of VEGF121 versus VEGF145, 165, and 189 is observed

    Journal: Cancer Microenvironment

    Article Title: Microenvironment Changes (in pH) Affect VEGF Alternative Splicing

    doi: 10.1007/s12307-008-0013-4

    Figure Lengend Snippet: Proposed model. When endometrial cancer cells are exposed to acidic medium the p38 MAPK signaling pathway is activated and an increase in SR proteins phosphorylation that will eventually regulate the VEGF alternative splicing takes place. In acidosis, not only VEGF expression is increased but also a modification of the alternative splicing occurs, where an increase in the proportion of VEGF121 versus VEGF145, 165, and 189 is observed

    Article Snippet: To test the importance of the different signaling pathways in the regulation of VEGF alternative splicing, the RL95 cell line was cultured in growth medium at pH 5.5 with or without the inhibitors of p38 MAPK (SB202190, Sigma, 20 µM,) and SAPK/JNK (SP600125, Sigma, 20 µM) signaling pathways.

    Techniques: Expressing, Modification

    a Correlation between VEGF isoforms pattern inversion and the activation of stress signaling pathways in acidic conditions. After 8 h of pH 5.5 stimulation, the changes in VEGF isoform splicing pattern are more pronounced. b As shown by western blotting and densitometry quantification, at this time point, from the several signaling pathways analyzed, only the p38 MAPK ( p

    Journal: Cancer Microenvironment

    Article Title: Microenvironment Changes (in pH) Affect VEGF Alternative Splicing

    doi: 10.1007/s12307-008-0013-4

    Figure Lengend Snippet: a Correlation between VEGF isoforms pattern inversion and the activation of stress signaling pathways in acidic conditions. After 8 h of pH 5.5 stimulation, the changes in VEGF isoform splicing pattern are more pronounced. b As shown by western blotting and densitometry quantification, at this time point, from the several signaling pathways analyzed, only the p38 MAPK ( p

    Article Snippet: To test the importance of the different signaling pathways in the regulation of VEGF alternative splicing, the RL95 cell line was cultured in growth medium at pH 5.5 with or without the inhibitors of p38 MAPK (SB202190, Sigma, 20 µM,) and SAPK/JNK (SP600125, Sigma, 20 µM) signaling pathways.

    Techniques: Activation Assay, Western Blot

    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

    Effect of the p38 MAPK inhibitor SB202190 on SOD3 mRNA expression. (a–c) The inhibition of p38 MAPK phosphorylation increased the SOD3 expression in human TPC1 and 8505c cells, while SB202190 treatment did not alter the SOD3 mRNA synthesis in Nthy cells modeling normal thyroid. (d–f) The inhibitor treatment increased sod3 mRNA expression in PC Cl3-derived PC PTC1 and PC E1A cells, while the treatment had no effect on PC Cl3 control cells modeling normal thyroid. (g–j) FRLT5 cell clones V13, V21, and V39 stably transfected with RAS showed a significant increase in sod3 mRNA expression after SB202190 treatment, whereas SB202190 had no effect on FRLT5 control cells, which is consistent with the results using the other cell models. (k, m) The Western blot analysis for p38 MAPK activation in FRLT5 control cells, clone V13, clone V21, and clone V39. The histogram (panel (m)) suggested significantly increased p38 MAPK phosphorylation in FRLT5-derived clones compared to control cells. Total p38 MAPK was used to normalize the phosphorylation level. (l, n) The transient transfection of an H-RasV12 expression plasmid into HEK 293T cells showed a gradual increase in p38 MAPK phosphorylation that corresponded to the amount of plasmid transfected. Total p38 MAPK was used to normalize the phosphorylation level. The data are expressed as the mean ± SD. The p values are represented ( ∗ p

    Journal: BioMed Research International

    Article Title: Ras Oncogene-Mediated Progressive Silencing of Extracellular Superoxide Dismutase in Tumorigenesis

    doi: 10.1155/2015/780409

    Figure Lengend Snippet: Effect of the p38 MAPK inhibitor SB202190 on SOD3 mRNA expression. (a–c) The inhibition of p38 MAPK phosphorylation increased the SOD3 expression in human TPC1 and 8505c cells, while SB202190 treatment did not alter the SOD3 mRNA synthesis in Nthy cells modeling normal thyroid. (d–f) The inhibitor treatment increased sod3 mRNA expression in PC Cl3-derived PC PTC1 and PC E1A cells, while the treatment had no effect on PC Cl3 control cells modeling normal thyroid. (g–j) FRLT5 cell clones V13, V21, and V39 stably transfected with RAS showed a significant increase in sod3 mRNA expression after SB202190 treatment, whereas SB202190 had no effect on FRLT5 control cells, which is consistent with the results using the other cell models. (k, m) The Western blot analysis for p38 MAPK activation in FRLT5 control cells, clone V13, clone V21, and clone V39. The histogram (panel (m)) suggested significantly increased p38 MAPK phosphorylation in FRLT5-derived clones compared to control cells. Total p38 MAPK was used to normalize the phosphorylation level. (l, n) The transient transfection of an H-RasV12 expression plasmid into HEK 293T cells showed a gradual increase in p38 MAPK phosphorylation that corresponded to the amount of plasmid transfected. Total p38 MAPK was used to normalize the phosphorylation level. The data are expressed as the mean ± SD. The p values are represented ( ∗ p

    Article Snippet: To study the regulation of sod3 gene expression, the cells were supplemented with 10 μ M 5-azacytidine (Sigma), 100 nM TSA (Sigma), and 10 μ M SB202190 p38 MAPK inhibitor (Sigma) for 24 hours or with H2 O2 (Sigma) for 6 hours.

    Techniques: Expressing, Inhibition, Derivative Assay, Clone Assay, Stable Transfection, Transfection, Western Blot, Activation Assay, Plasmid Preparation

    Effect of p38 MAPK inhibitor SB202190 (FHPI) on CAT expression from the UL4-CAT promoter in recombinant virus-infected HFFs. Confluent HFFs were serum starved for 24 h and then treated with FHPI for 1 h before infection with various recombinant viruses in the presence of FHPI in quadruplicate as described in Materials and Methods. Cells were harvested at 14 h after infection and subjected to CAT assays. The results of the CAT assays were averaged, and the standard deviations were calculated. The CAT activity per microgram of protein at various concentrations of the drug is relative to that of the nontreated recombinant viruses.

    Journal: Journal of Virology

    Article Title: Role of Regulatory Elements and the MAPK/ERK or p38 MAPK Pathways for Activation of Human Cytomegalovirus Gene Expression

    doi: 10.1128/JVI.76.10.4873-4885.2002

    Figure Lengend Snippet: Effect of p38 MAPK inhibitor SB202190 (FHPI) on CAT expression from the UL4-CAT promoter in recombinant virus-infected HFFs. Confluent HFFs were serum starved for 24 h and then treated with FHPI for 1 h before infection with various recombinant viruses in the presence of FHPI in quadruplicate as described in Materials and Methods. Cells were harvested at 14 h after infection and subjected to CAT assays. The results of the CAT assays were averaged, and the standard deviations were calculated. The CAT activity per microgram of protein at various concentrations of the drug is relative to that of the nontreated recombinant viruses.

    Article Snippet: For infection of HFFs in the presence of the MEK inhibitor UO126 (Promega) or the p38 MAPK inhibitor SB202190 (FHPI) (Calbiochem Corp., San Diego, Calif.), the drugs were dissolved in dimethyl sulfoxide (DMSO) to make a 10 mM stock as recommended by the manufacturer.

    Techniques: Expressing, Recombinant, Infection, Activity Assay

    Effect of KM11073 on the activation of p38. Cells (1 × 10 5 cells/well) were cultured in a 6-well plate for 1 day and then incubated with DMEM containing 5% FBS in the presence or absence of BMP-2 and/or KM11073 ( A ). Inhibitory effects of p38 inhibitors (1, SB202190; 2, PD169316; 3, SB203580) on the activation of p38 by BMP-2 and KM11073. Western blot analysis was performed with protein samples prepared with cells treated with each inhibitor for 30 min and then incubated with BMP-2 and KM11073 for 30 min ( B ). The relative, normalized ratio between phosphorylated protein and the protein itself was presented.

    Journal: PLoS ONE

    Article Title: Quinoline Compound KM11073 Enhances BMP-2-Dependent Osteogenic Differentiation of C2C12 Cells via Activation of p38 Signaling and Exhibits In Vivo Bone Forming Activity

    doi: 10.1371/journal.pone.0120150

    Figure Lengend Snippet: Effect of KM11073 on the activation of p38. Cells (1 × 10 5 cells/well) were cultured in a 6-well plate for 1 day and then incubated with DMEM containing 5% FBS in the presence or absence of BMP-2 and/or KM11073 ( A ). Inhibitory effects of p38 inhibitors (1, SB202190; 2, PD169316; 3, SB203580) on the activation of p38 by BMP-2 and KM11073. Western blot analysis was performed with protein samples prepared with cells treated with each inhibitor for 30 min and then incubated with BMP-2 and KM11073 for 30 min ( B ). The relative, normalized ratio between phosphorylated protein and the protein itself was presented.

    Article Snippet: Ras inhibitor FTI-277, PI3K inhibitor LY294002, Akt inhibitor, and p38 inhibitors (PD169316, SB203581, and SB202190) were purchased from Calbiochem (EMD Biosciences, Inc., La Jolla, CA, USA).

    Techniques: Activation Assay, Cell Culture, Incubation, Western Blot

    Involvement of p38 in the KM11073-mediated enhancement of BMP-2-stimulated ALP induction. In a 96-well plate, cells (4 × 10 3 cells/well) were treated with each inhibitor for 2 h and then treated with BMP-2 and KM11073. After 3 days, the cells were treated with each inhibitor. On differentiation day 6, ALP staining (A) and its activity (B) were assayed. ### p

    Journal: PLoS ONE

    Article Title: Quinoline Compound KM11073 Enhances BMP-2-Dependent Osteogenic Differentiation of C2C12 Cells via Activation of p38 Signaling and Exhibits In Vivo Bone Forming Activity

    doi: 10.1371/journal.pone.0120150

    Figure Lengend Snippet: Involvement of p38 in the KM11073-mediated enhancement of BMP-2-stimulated ALP induction. In a 96-well plate, cells (4 × 10 3 cells/well) were treated with each inhibitor for 2 h and then treated with BMP-2 and KM11073. After 3 days, the cells were treated with each inhibitor. On differentiation day 6, ALP staining (A) and its activity (B) were assayed. ### p

    Article Snippet: Ras inhibitor FTI-277, PI3K inhibitor LY294002, Akt inhibitor, and p38 inhibitors (PD169316, SB203581, and SB202190) were purchased from Calbiochem (EMD Biosciences, Inc., La Jolla, CA, USA).

    Techniques: ALP Assay, Staining, Activity Assay

    Effects of non-Smad signaling on Dkk1 and Sost expression in osteoblasts. ( A ) Effects of p38 MAPK inhibitor SB202190 on Dkk1 and Sost expression using primary osteoblasts from newborn wild-type mice as assessed by qRT-PCR. mRNA was isolated from wild-type osteoblasts pretreated with SB202190 (10 µM) or DMSO in the absence of serum for 1 hour prior to the addition of BMP2 (100 ng/mL) or PBS for 3 hours. Upregulation of Dkk1 expression by BMP2 treatment was restored by SB202190 pretreatment. Sost expression was increased significantly by BMP2 treatment with SB202190 pretreatment. Values are expressed relative to untreated osteoblasts (neither SB202190 nor BMP2) (mean ± SD; t test; * p

    Journal: Journal of Bone and Mineral Research

    Article Title: Wnt Inhibitors Dkk1 and Sost Are Downstream Targets of BMP Signaling Through the Type IA Receptor (BMPRIA) in Osteoblasts

    doi: 10.1359/jbmr.090806

    Figure Lengend Snippet: Effects of non-Smad signaling on Dkk1 and Sost expression in osteoblasts. ( A ) Effects of p38 MAPK inhibitor SB202190 on Dkk1 and Sost expression using primary osteoblasts from newborn wild-type mice as assessed by qRT-PCR. mRNA was isolated from wild-type osteoblasts pretreated with SB202190 (10 µM) or DMSO in the absence of serum for 1 hour prior to the addition of BMP2 (100 ng/mL) or PBS for 3 hours. Upregulation of Dkk1 expression by BMP2 treatment was restored by SB202190 pretreatment. Sost expression was increased significantly by BMP2 treatment with SB202190 pretreatment. Values are expressed relative to untreated osteoblasts (neither SB202190 nor BMP2) (mean ± SD; t test; * p

    Article Snippet: Wild-type osteoblasts also were pretreated with dorsomorphin (10 µM), p38 mitogen-activated protein kinase (MAPK) inhibitor SB202190 (10 µM, Calbiochem, Gibbstown, NJ, USA), and DMSO in the absence of serum for 1 hour before BMP2 treatment (100 ng/mL).

    Techniques: Expressing, Mouse Assay, Quantitative RT-PCR, Isolation

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

    Journal: PLoS ONE

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

    doi: 10.1371/journal.pone.0007875

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

    Article Snippet: To identify kinase pathways that were driving basal hepcidin expression in cultured cells in the presence of FCS, the following inhibitors were used: the phosphatidylinositol 3 kinase (PI3K) inhibitor LY294002 (10 µM, Calbiochem), the p38 stress-activated protein kinase (SAPK) inhibitor SB202190 (10 µM, Sigma), the mitogen-activated protein kinase kinase (MEK)1/2 inhibitor UO126 (1 µM, Cell Signaling) and the pan kinase inhibitor staurosporine (0.5 µM, Sigma).

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