sb202190  (Abcam)

 
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    Name:
    SB 202190
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    ab120638
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    Structured Review

    Abcam sb202190
    Phospho-p38 MAPK inhibitors prevent and reverse EndoMT-associated gene expression in vitro. ( a ) To study possible prevention of EndoMT, hREC were treated with the p38 MAPK inhibitor SB203580 or <t>SB202190</t> (10 μM) during EndoMT induction. Expression levels for the genes encoding the EndoMT-associated proteins SNAI1, SNAI2, α-SMA, FSP-1, vimentin, fibronectin, COL1A2 and COL3A1; and the endothelial differentiation markers VE-cadherin, CD31 and VEGFR2 were assessed by qPCR on day 6 of EndoMT induction. Data = mean ± SEM, * p

    https://www.bioz.com/result/sb202190/product/Abcam
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    sb202190 - by Bioz Stars, 2021-03
    94/100 stars

    Images

    1) Product Images from "Fibrotic Changes and Endothelial-to-Mesenchymal Transition Promoted by VEGFR2 Antagonism Alter the Therapeutic Effects of VEGFA Pathway Blockage in a Mouse Model of Choroidal Neovascularization"

    Article Title: Fibrotic Changes and Endothelial-to-Mesenchymal Transition Promoted by VEGFR2 Antagonism Alter the Therapeutic Effects of VEGFA Pathway Blockage in a Mouse Model of Choroidal Neovascularization

    Journal: Cells

    doi: 10.3390/cells9092057

    Phospho-p38 MAPK inhibitors prevent and reverse EndoMT-associated gene expression in vitro. ( a ) To study possible prevention of EndoMT, hREC were treated with the p38 MAPK inhibitor SB203580 or SB202190 (10 μM) during EndoMT induction. Expression levels for the genes encoding the EndoMT-associated proteins SNAI1, SNAI2, α-SMA, FSP-1, vimentin, fibronectin, COL1A2 and COL3A1; and the endothelial differentiation markers VE-cadherin, CD31 and VEGFR2 were assessed by qPCR on day 6 of EndoMT induction. Data = mean ± SEM, * p
    Figure Legend Snippet: Phospho-p38 MAPK inhibitors prevent and reverse EndoMT-associated gene expression in vitro. ( a ) To study possible prevention of EndoMT, hREC were treated with the p38 MAPK inhibitor SB203580 or SB202190 (10 μM) during EndoMT induction. Expression levels for the genes encoding the EndoMT-associated proteins SNAI1, SNAI2, α-SMA, FSP-1, vimentin, fibronectin, COL1A2 and COL3A1; and the endothelial differentiation markers VE-cadherin, CD31 and VEGFR2 were assessed by qPCR on day 6 of EndoMT induction. Data = mean ± SEM, * p

    Techniques Used: Expressing, In Vitro, Real-time Polymerase Chain Reaction

    2) Product Images from "TGF-β regulates phosphorylation and stabilization of Sox9 protein in chondrocytes through p38 and Smad dependent mechanisms"

    Article Title: TGF-β regulates phosphorylation and stabilization of Sox9 protein in chondrocytes through p38 and Smad dependent mechanisms

    Journal: Scientific Reports

    doi: 10.1038/srep38616

    Phosphorylation of Sox9 and up-regulation of Sox9 protein by TGF-β1 is dependent on p38 activity. ( A , B ) ATDC5 cells were pretreated with different concentrations of SB203580 ( A ) and SB202190 ( B ). After 24 hours, cells were treated with vehicle control (−) or TGF-β1 (+) for 24 hours. Cell lysates were used in immunblots to measure p-MAPK-APK2 protein levels. N = 3. ( C ) Cells were pretreated with 10 μM SB203580 (p38i 1), 5 μM SB202190 (p38i 2), or DMSO control for 24 hours, and TGF-β1 (+) or vehicle control (−) was added to the cells, which were incubated for an additional 2 hours. Cell lysates were used in immunoblots to detect p-Sox9 protein, N = 4. ( D ) Cell lysates were also collected 6 hours after treatment with TGF-β1 (+) or vehicle control (−) and used to determine Sox9 protein levels, N = 6. ( E ) Sox9 mRNA levels were measured in cells that were pretreated with p38i 1, p38i 2, or DMSO and then treated with TGF-β1 or vehicle for 6 hours, N = 5. ( F ) ATDC5 cells were transfected with 30 pmol of p38α and p38β siRNA or N.S. siRNA. After 48 hours, cells were treated with TGF-β1 for 2 or 6 hours. Protein lysates were collected and p-Sox9 and Sox9 protein levels were determined by immunoblot, N = 3. ( G ) Papss2 mRNA levels were measured by QPCR after pretreatment with DMSO or p38i followed by treatment with TGF-β1 or vehicle. mRNA levels were determined relative to DMSO/vehicle treated samples. PPIA was used for gene expression normalization. All QPCR data was analyzed using REST software. *** p > 0.001, N = 4. Western blots were cropped for clarity. Examples of uncropped blots are found in Supplementary Figure S4 .
    Figure Legend Snippet: Phosphorylation of Sox9 and up-regulation of Sox9 protein by TGF-β1 is dependent on p38 activity. ( A , B ) ATDC5 cells were pretreated with different concentrations of SB203580 ( A ) and SB202190 ( B ). After 24 hours, cells were treated with vehicle control (−) or TGF-β1 (+) for 24 hours. Cell lysates were used in immunblots to measure p-MAPK-APK2 protein levels. N = 3. ( C ) Cells were pretreated with 10 μM SB203580 (p38i 1), 5 μM SB202190 (p38i 2), or DMSO control for 24 hours, and TGF-β1 (+) or vehicle control (−) was added to the cells, which were incubated for an additional 2 hours. Cell lysates were used in immunoblots to detect p-Sox9 protein, N = 4. ( D ) Cell lysates were also collected 6 hours after treatment with TGF-β1 (+) or vehicle control (−) and used to determine Sox9 protein levels, N = 6. ( E ) Sox9 mRNA levels were measured in cells that were pretreated with p38i 1, p38i 2, or DMSO and then treated with TGF-β1 or vehicle for 6 hours, N = 5. ( F ) ATDC5 cells were transfected with 30 pmol of p38α and p38β siRNA or N.S. siRNA. After 48 hours, cells were treated with TGF-β1 for 2 or 6 hours. Protein lysates were collected and p-Sox9 and Sox9 protein levels were determined by immunoblot, N = 3. ( G ) Papss2 mRNA levels were measured by QPCR after pretreatment with DMSO or p38i followed by treatment with TGF-β1 or vehicle. mRNA levels were determined relative to DMSO/vehicle treated samples. PPIA was used for gene expression normalization. All QPCR data was analyzed using REST software. *** p > 0.001, N = 4. Western blots were cropped for clarity. Examples of uncropped blots are found in Supplementary Figure S4 .

    Techniques Used: Activity Assay, Incubation, Western Blot, Transfection, Real-time Polymerase Chain Reaction, Expressing, Software

    3) Product Images from "Fibrotic Changes and Endothelial-to-Mesenchymal Transition Promoted by VEGFR2 Antagonism Alter the Therapeutic Effects of VEGFA Pathway Blockage in a Mouse Model of Choroidal Neovascularization"

    Article Title: Fibrotic Changes and Endothelial-to-Mesenchymal Transition Promoted by VEGFR2 Antagonism Alter the Therapeutic Effects of VEGFA Pathway Blockage in a Mouse Model of Choroidal Neovascularization

    Journal: Cells

    doi: 10.3390/cells9092057

    Phospho-p38 MAPK inhibitors prevent and reverse EndoMT-associated gene expression in vitro. ( a ) To study possible prevention of EndoMT, hREC were treated with the p38 MAPK inhibitor SB203580 or SB202190 (10 μM) during EndoMT induction. Expression levels for the genes encoding the EndoMT-associated proteins SNAI1, SNAI2, α-SMA, FSP-1, vimentin, fibronectin, COL1A2 and COL3A1; and the endothelial differentiation markers VE-cadherin, CD31 and VEGFR2 were assessed by qPCR on day 6 of EndoMT induction. Data = mean ± SEM, * p
    Figure Legend Snippet: Phospho-p38 MAPK inhibitors prevent and reverse EndoMT-associated gene expression in vitro. ( a ) To study possible prevention of EndoMT, hREC were treated with the p38 MAPK inhibitor SB203580 or SB202190 (10 μM) during EndoMT induction. Expression levels for the genes encoding the EndoMT-associated proteins SNAI1, SNAI2, α-SMA, FSP-1, vimentin, fibronectin, COL1A2 and COL3A1; and the endothelial differentiation markers VE-cadherin, CD31 and VEGFR2 were assessed by qPCR on day 6 of EndoMT induction. Data = mean ± SEM, * p

    Techniques Used: Expressing, In Vitro, Real-time Polymerase Chain Reaction

    4) Product Images from "CXCL12/CXCR4 Axis Regulates Aggrecanase Activation and Cartilage Degradation in a Post-Traumatic Osteoarthritis Rat Model"

    Article Title: CXCL12/CXCR4 Axis Regulates Aggrecanase Activation and Cartilage Degradation in a Post-Traumatic Osteoarthritis Rat Model

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms17101522

    CXCL12a upregulates the activation of the Wnt/β-catenin pathway and blocking the MAPK or Wnt-catenin inhibits CXCL12a-induced expression of RUNX-2, and ADAMTS-4/5 and enhances the expression of SOX-9, and the model of CXCL12/CXCR4 axis-induced activation of aggrecanases. ( a ) Starved primary chondrocytes were exposed to CXCL12a (250 ng/mL), siRNA targeting CXCR4, CXCL12a + NC or CXCL12a + siRNA targeting CXCR4 for 48 h. The expression of molecules related to the Wnt/β-catenin pathway was demonstrated by the Western blotting assay; ( b ) The relative expression of β-catenin in different subcellular fractions was compared. β-Catenin and PCNA served as loading controls ( n = 4 for each group); ( c ) Primary chondrocytes were cultured in the presence of empty control, CXCL12a, SB202190/U-0126 + CXCL12a, or C59 + CXCL12a for 72 h, and subjected to Western blot analyses to evaluate the protein levels of ADAMTS-4/5, ACAN, SOX-9, and RUNX-2. β-catenin served as a loading control ( n = 4 for each group); and ( d ) CXCL12a produced in synovial fibroblasts binds to CXCR4 expressed by chondrocytes and subsequently activates the Wnt/β-catenin pathway, and leads to NF-κB activation and the phosphorylation of MAPKs, which are partly responsible for the increased expression of RUNX-2 and the downregulation of SOX-9. These changes ultimately promote the expression of aggrecanases.
    Figure Legend Snippet: CXCL12a upregulates the activation of the Wnt/β-catenin pathway and blocking the MAPK or Wnt-catenin inhibits CXCL12a-induced expression of RUNX-2, and ADAMTS-4/5 and enhances the expression of SOX-9, and the model of CXCL12/CXCR4 axis-induced activation of aggrecanases. ( a ) Starved primary chondrocytes were exposed to CXCL12a (250 ng/mL), siRNA targeting CXCR4, CXCL12a + NC or CXCL12a + siRNA targeting CXCR4 for 48 h. The expression of molecules related to the Wnt/β-catenin pathway was demonstrated by the Western blotting assay; ( b ) The relative expression of β-catenin in different subcellular fractions was compared. β-Catenin and PCNA served as loading controls ( n = 4 for each group); ( c ) Primary chondrocytes were cultured in the presence of empty control, CXCL12a, SB202190/U-0126 + CXCL12a, or C59 + CXCL12a for 72 h, and subjected to Western blot analyses to evaluate the protein levels of ADAMTS-4/5, ACAN, SOX-9, and RUNX-2. β-catenin served as a loading control ( n = 4 for each group); and ( d ) CXCL12a produced in synovial fibroblasts binds to CXCR4 expressed by chondrocytes and subsequently activates the Wnt/β-catenin pathway, and leads to NF-κB activation and the phosphorylation of MAPKs, which are partly responsible for the increased expression of RUNX-2 and the downregulation of SOX-9. These changes ultimately promote the expression of aggrecanases.

    Techniques Used: Activation Assay, Blocking Assay, Expressing, Western Blot, Cell Culture, Produced

    5) Product Images from "Fibrotic Changes and Endothelial-to-Mesenchymal Transition Promoted by VEGFR2 Antagonism Alter the Therapeutic Effects of VEGFA Pathway Blockage in a Mouse Model of Choroidal Neovascularization"

    Article Title: Fibrotic Changes and Endothelial-to-Mesenchymal Transition Promoted by VEGFR2 Antagonism Alter the Therapeutic Effects of VEGFA Pathway Blockage in a Mouse Model of Choroidal Neovascularization

    Journal: Cells

    doi: 10.3390/cells9092057

    Phospho-p38 MAPK inhibitors prevent and reverse EndoMT-associated gene expression in vitro. ( a ) To study possible prevention of EndoMT, hREC were treated with the p38 MAPK inhibitor SB203580 or SB202190 (10 μM) during EndoMT induction. Expression levels for the genes encoding the EndoMT-associated proteins SNAI1, SNAI2, α-SMA, FSP-1, vimentin, fibronectin, COL1A2 and COL3A1; and the endothelial differentiation markers VE-cadherin, CD31 and VEGFR2 were assessed by qPCR on day 6 of EndoMT induction. Data = mean ± SEM, * p
    Figure Legend Snippet: Phospho-p38 MAPK inhibitors prevent and reverse EndoMT-associated gene expression in vitro. ( a ) To study possible prevention of EndoMT, hREC were treated with the p38 MAPK inhibitor SB203580 or SB202190 (10 μM) during EndoMT induction. Expression levels for the genes encoding the EndoMT-associated proteins SNAI1, SNAI2, α-SMA, FSP-1, vimentin, fibronectin, COL1A2 and COL3A1; and the endothelial differentiation markers VE-cadherin, CD31 and VEGFR2 were assessed by qPCR on day 6 of EndoMT induction. Data = mean ± SEM, * p

    Techniques Used: Expressing, In Vitro, Real-time Polymerase Chain Reaction

    Related Articles

    Irradiation:

    Article Title: Functional Dissection of the Enhancer Repertoire in Human Embryonic Stem Cells
    Article Snippet: For transfection, single cells were obtained by Accutase treatment (Invitrogen, A1110501), in the presence of Rock inhibitor, Y-27632 (10uM, Cambridge bioscience, SM02-10). .. For conversion to the naive state, cells were split on irradiated MEFs on gelatin coated plates and media was changed to NHSM media, as described by , containing knockout DMEM (Invitrogen), 20% knockout serum (Invitrogen), human insulin (Sigma, 12.5 μg ml-1 final concentration), 20 ng ml-1 recombinant human LIF (Millipore), 8 ng ml-1 recombinant bFGF (Peprotech) and 1 ng ml-1 recombinant TGF-β1 (Peprotech), 1 mM glutamine (Invitrogen), 1% nonessential amino acids (Invitrogen), 0.1 mM beta-mercaptoethanol (Invitrogen), penicillin-streptomycin (Invitrogen) and small molecule inhibitors: PD0325901 (1 μM, ERK1/2i, Axon Medchem); CHIR99021 (3 μM, GSKβi, Axon Medchem); SP600125 (10 μM, JNKi, Abcam ab120065) and SB203580 (10 μM, p38i,Abcam ab120638) Y-27632 (5 μM, ROCKi) and protein kinase C inhibitor G06983 (5 μM, PKCi, Abcam, ab144414). .. Cells were 1:10 passaged using TrypLE™ (Invitrogen, 12604021) in the presence of Rock inhibitor and maintained for more than 10 passages in NHSM media prior to analysis.

    Knock-Out:

    Article Title: Functional Dissection of the Enhancer Repertoire in Human Embryonic Stem Cells
    Article Snippet: For transfection, single cells were obtained by Accutase treatment (Invitrogen, A1110501), in the presence of Rock inhibitor, Y-27632 (10uM, Cambridge bioscience, SM02-10). .. For conversion to the naive state, cells were split on irradiated MEFs on gelatin coated plates and media was changed to NHSM media, as described by , containing knockout DMEM (Invitrogen), 20% knockout serum (Invitrogen), human insulin (Sigma, 12.5 μg ml-1 final concentration), 20 ng ml-1 recombinant human LIF (Millipore), 8 ng ml-1 recombinant bFGF (Peprotech) and 1 ng ml-1 recombinant TGF-β1 (Peprotech), 1 mM glutamine (Invitrogen), 1% nonessential amino acids (Invitrogen), 0.1 mM beta-mercaptoethanol (Invitrogen), penicillin-streptomycin (Invitrogen) and small molecule inhibitors: PD0325901 (1 μM, ERK1/2i, Axon Medchem); CHIR99021 (3 μM, GSKβi, Axon Medchem); SP600125 (10 μM, JNKi, Abcam ab120065) and SB203580 (10 μM, p38i,Abcam ab120638) Y-27632 (5 μM, ROCKi) and protein kinase C inhibitor G06983 (5 μM, PKCi, Abcam, ab144414). .. Cells were 1:10 passaged using TrypLE™ (Invitrogen, 12604021) in the presence of Rock inhibitor and maintained for more than 10 passages in NHSM media prior to analysis.

    Concentration Assay:

    Article Title: Functional Dissection of the Enhancer Repertoire in Human Embryonic Stem Cells
    Article Snippet: For transfection, single cells were obtained by Accutase treatment (Invitrogen, A1110501), in the presence of Rock inhibitor, Y-27632 (10uM, Cambridge bioscience, SM02-10). .. For conversion to the naive state, cells were split on irradiated MEFs on gelatin coated plates and media was changed to NHSM media, as described by , containing knockout DMEM (Invitrogen), 20% knockout serum (Invitrogen), human insulin (Sigma, 12.5 μg ml-1 final concentration), 20 ng ml-1 recombinant human LIF (Millipore), 8 ng ml-1 recombinant bFGF (Peprotech) and 1 ng ml-1 recombinant TGF-β1 (Peprotech), 1 mM glutamine (Invitrogen), 1% nonessential amino acids (Invitrogen), 0.1 mM beta-mercaptoethanol (Invitrogen), penicillin-streptomycin (Invitrogen) and small molecule inhibitors: PD0325901 (1 μM, ERK1/2i, Axon Medchem); CHIR99021 (3 μM, GSKβi, Axon Medchem); SP600125 (10 μM, JNKi, Abcam ab120065) and SB203580 (10 μM, p38i,Abcam ab120638) Y-27632 (5 μM, ROCKi) and protein kinase C inhibitor G06983 (5 μM, PKCi, Abcam, ab144414). .. Cells were 1:10 passaged using TrypLE™ (Invitrogen, 12604021) in the presence of Rock inhibitor and maintained for more than 10 passages in NHSM media prior to analysis.

    Article Title: p38 MAPK Is Activated but Does Not Play a Key Role during Apoptosis Induction by Saturated Fatty Acid in Human Pancreatic β-Cells
    Article Snippet: After 48 h of incubation with or without SA, the number of living cells was determined using a hemocytometer counting system after staining with trypan blue. .. Inhibitor and Activator Application Cells (approximately 5 × 105 cells per sample) were seeded and after a 24-h pre-incubation period (allowing cells to attach) the culture medium was replaced with: (1) a serum-free medium with or without the p38 MAPK inhibitor SB202190 (Abcam, Cambridge, UK) at a desired concentration; (2) a serum-free medium containing 2% BSA with or without the p38 MAPK activator anisomycin (Sigma Aldrich, St. Louis, MO, USA) at required concentration; or (3) a serum-free medium containing 2% BSA and SA. ..

    Recombinant:

    Article Title: Functional Dissection of the Enhancer Repertoire in Human Embryonic Stem Cells
    Article Snippet: For transfection, single cells were obtained by Accutase treatment (Invitrogen, A1110501), in the presence of Rock inhibitor, Y-27632 (10uM, Cambridge bioscience, SM02-10). .. For conversion to the naive state, cells were split on irradiated MEFs on gelatin coated plates and media was changed to NHSM media, as described by , containing knockout DMEM (Invitrogen), 20% knockout serum (Invitrogen), human insulin (Sigma, 12.5 μg ml-1 final concentration), 20 ng ml-1 recombinant human LIF (Millipore), 8 ng ml-1 recombinant bFGF (Peprotech) and 1 ng ml-1 recombinant TGF-β1 (Peprotech), 1 mM glutamine (Invitrogen), 1% nonessential amino acids (Invitrogen), 0.1 mM beta-mercaptoethanol (Invitrogen), penicillin-streptomycin (Invitrogen) and small molecule inhibitors: PD0325901 (1 μM, ERK1/2i, Axon Medchem); CHIR99021 (3 μM, GSKβi, Axon Medchem); SP600125 (10 μM, JNKi, Abcam ab120065) and SB203580 (10 μM, p38i,Abcam ab120638) Y-27632 (5 μM, ROCKi) and protein kinase C inhibitor G06983 (5 μM, PKCi, Abcam, ab144414). .. Cells were 1:10 passaged using TrypLE™ (Invitrogen, 12604021) in the presence of Rock inhibitor and maintained for more than 10 passages in NHSM media prior to analysis.

    Expressing:

    Article Title: Fibrotic Changes and Endothelial-to-Mesenchymal Transition Promoted by VEGFR2 Antagonism Alter the Therapeutic Effects of VEGFA Pathway Blockage in a Mouse Model of Choroidal Neovascularization
    Article Snippet: The numbers of live cells were determined by hemocytometer counting following trypan blue staining. .. For the prevention study using the p38 MAPK inhibitors, SB203580 or SB202190 (10 μM, Abcam, Cambridge, MA, USA) was applied with the pro-inflammatory cytokines at the beginning of induction and again at day three; expression of endothelial and EndoMT markers was analyzed by RT-qPCR at day six. .. For the intervention study, SB203580 was added at days six, nine and 12 post-induction, and gene expression was analyzed at day 15.

    Article Title: Fibrotic Changes and Endothelial-to-Mesenchymal Transition Promoted by VEGFR2 Antagonism Alter the Therapeutic Effects of VEGFA Pathway Blockage in a Mouse Model of Choroidal Neovascularization
    Article Snippet: Both drugs were used at 10 µM final concentration based on a pilot dose escalation study in which this dose and a higher dose (20 µM) yielded similar levels of EndoMT suppression and expression of markers associated with differentiated endothelial cells ( ). .. In the prevention study, both SB203580 and SB202190 suppressed cytokine-induced expression of the EndoMT-associated genes encoding SNAI1, SNAI2, vimentin, fibronectin, COL1A2, and COL3A1 (p < 0.05 to p < 0.001, a), though neither prevented the increase in expression of the genes encoding α-SMA and FSP-1. .. However, only SB203580 preserved expression of the full set of endothelial differentiation markers (p < 0.01 to p < 0.001 for the increase in expression of CD31, VE-cadherin, and VEGFR2 relative to EndoMT); SB202190 preserved expression only of VEGFR2 (p< 0.001 compared to EndoMT).

    Quantitative RT-PCR:

    Article Title: Fibrotic Changes and Endothelial-to-Mesenchymal Transition Promoted by VEGFR2 Antagonism Alter the Therapeutic Effects of VEGFA Pathway Blockage in a Mouse Model of Choroidal Neovascularization
    Article Snippet: The numbers of live cells were determined by hemocytometer counting following trypan blue staining. .. For the prevention study using the p38 MAPK inhibitors, SB203580 or SB202190 (10 μM, Abcam, Cambridge, MA, USA) was applied with the pro-inflammatory cytokines at the beginning of induction and again at day three; expression of endothelial and EndoMT markers was analyzed by RT-qPCR at day six. .. For the intervention study, SB203580 was added at days six, nine and 12 post-induction, and gene expression was analyzed at day 15.

    other:

    Article Title: p38 MAPK Is Activated but Does Not Play a Key Role during Apoptosis Induction by Saturated Fatty Acid in Human Pancreatic β-Cells
    Article Snippet: The p38 MAPK inhibitor SB202190, the activator anisomycin, and SA were applied in the same way as described above (“Inhibitor and activator application”).

    Article Title: Fibrotic Changes and Endothelial-to-Mesenchymal Transition Promoted by VEGFR2 Antagonism Alter the Therapeutic Effects of VEGFA Pathway Blockage in a Mouse Model of Choroidal Neovascularization
    Article Snippet: The inhibitors SB203580 and SB202190 (both are p38α- and p38β2-selective inhibitors) have specificities and potencies against different MAPK family members, namely p38α, p38β, p38γ and p38δ [ , ], and were added either together with the cytokines used to induce EndoMT (prevention study) or six days after induction of EndoMT (intervention study).

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    Abcam p38 mapk inhibitor sb202190
    Effect of <t>p38</t> <t>MAPK</t> silencing, using a specific siRNA (see “Materials and Methods”) and the effect of stearic acid (SA), on ( A ) the level of p38 MAPK, phospho-p38 MAPK, phospho-MAPKAPK-2 (substrate of p38 MAPK); ( B ) the level of phospho-c-Raf, phospho-MEK1/2, phospho-ERK1/2 (the ERK signaling pathway); and ( C ) cell growth and viability of NES2Y cells. Cells incubated without siRNA represented control cells. After 18 h of incubation (see “Materials and Methods”) with or without stearic acid (SA) ( A , B ), the level of individual proteins was determined using Western blot analysis and the relevant antibodies (see “Materials and Methods”). A monoclonal antibody against human actin was used to confirm equal protein loading. The data shown were obtained in one representative experiment from three independent experiments. When assessing cell growth and viability ( C ), cells were seeded at a concentration of 2 × 10 4 cells/100 µL of culture medium per well of 96-well plate (see “Materials and Methods”). The number of living cells was determined after 48 h of incubation with or without SA. Non-specific siRNA was used as a negative control. Each column represents the mean of four separate cultures ± SEM. NS (non-significant) when comparing the number of cells incubated with p38 MAPK specific siRNA and with non-specific siRNA.
    P38 Mapk Inhibitor Sb202190, supplied by Abcam, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p38 mapk inhibitor sb202190/product/Abcam
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p38 mapk inhibitor sb202190 - by Bioz Stars, 2021-03
    94/100 stars
      Buy from Supplier

    Image Search Results


    Effect of p38 MAPK silencing, using a specific siRNA (see “Materials and Methods”) and the effect of stearic acid (SA), on ( A ) the level of p38 MAPK, phospho-p38 MAPK, phospho-MAPKAPK-2 (substrate of p38 MAPK); ( B ) the level of phospho-c-Raf, phospho-MEK1/2, phospho-ERK1/2 (the ERK signaling pathway); and ( C ) cell growth and viability of NES2Y cells. Cells incubated without siRNA represented control cells. After 18 h of incubation (see “Materials and Methods”) with or without stearic acid (SA) ( A , B ), the level of individual proteins was determined using Western blot analysis and the relevant antibodies (see “Materials and Methods”). A monoclonal antibody against human actin was used to confirm equal protein loading. The data shown were obtained in one representative experiment from three independent experiments. When assessing cell growth and viability ( C ), cells were seeded at a concentration of 2 × 10 4 cells/100 µL of culture medium per well of 96-well plate (see “Materials and Methods”). The number of living cells was determined after 48 h of incubation with or without SA. Non-specific siRNA was used as a negative control. Each column represents the mean of four separate cultures ± SEM. NS (non-significant) when comparing the number of cells incubated with p38 MAPK specific siRNA and with non-specific siRNA.

    Journal: International Journal of Molecular Sciences

    Article Title: p38 MAPK Is Activated but Does Not Play a Key Role during Apoptosis Induction by Saturated Fatty Acid in Human Pancreatic β-Cells

    doi: 10.3390/ijms17020159

    Figure Lengend Snippet: Effect of p38 MAPK silencing, using a specific siRNA (see “Materials and Methods”) and the effect of stearic acid (SA), on ( A ) the level of p38 MAPK, phospho-p38 MAPK, phospho-MAPKAPK-2 (substrate of p38 MAPK); ( B ) the level of phospho-c-Raf, phospho-MEK1/2, phospho-ERK1/2 (the ERK signaling pathway); and ( C ) cell growth and viability of NES2Y cells. Cells incubated without siRNA represented control cells. After 18 h of incubation (see “Materials and Methods”) with or without stearic acid (SA) ( A , B ), the level of individual proteins was determined using Western blot analysis and the relevant antibodies (see “Materials and Methods”). A monoclonal antibody against human actin was used to confirm equal protein loading. The data shown were obtained in one representative experiment from three independent experiments. When assessing cell growth and viability ( C ), cells were seeded at a concentration of 2 × 10 4 cells/100 µL of culture medium per well of 96-well plate (see “Materials and Methods”). The number of living cells was determined after 48 h of incubation with or without SA. Non-specific siRNA was used as a negative control. Each column represents the mean of four separate cultures ± SEM. NS (non-significant) when comparing the number of cells incubated with p38 MAPK specific siRNA and with non-specific siRNA.

    Article Snippet: The p38 MAPK inhibitor SB202190, the activator anisomycin, and SA were applied in the same way as described above (“Inhibitor and activator application”).

    Techniques: Incubation, Western Blot, Concentration Assay, Negative Control

    Effect of p38 MAPK overexpression, using transfection with a specific plasmid (Vector with p38 MAPK) (see “Materials and Methods”) and the effect of stearic acid (SA) on ( A ) the level of p38 MAPK, phospho-p38 MAPK and phospho-MAPKAPK-2 (substrate of p38 MAPK); ( B ) the level of phospho-c-Raf, phospho-MEK1/2, phospho-ERK1/2 (the ERK signaling pathway); and ( C ) cell growth and viability of NES2Y cells. Cells transfected with an empty vector (Empty vector) represented control cells. After 18 h of incubation (see “Materials and Methods”) with or without stearic acid (SA) ( A , B ), the level of individual proteins was determined using Western blot analysis and the relevant antibodies (see “Materials and Methods”). A monoclonal antibody against human actin was used to confirm equal protein loading. The data shown were obtained in one representative experiment from three independent experiments. The fact that the band of p38 MAPK in the control samples is not visible here resulted from a large difference in p38 MAPK content in control and transfected cells. When assessing cell growth and viability ( C ), cells were seeded at a concentration of 2 × 10 4 cells/100 µL of culture medium per well of 96-well plate (see “Materials and Methods”). The number of living cells was determined after 48 h of incubation with or without SA. Each column represents the mean of four separate cultures ± SEM. NS (non-significant) when comparing the number of cells incubated with plasmid DNA containing p38 MAPK (Vector with p38 MAPK) and cells incubated with empty plasmid DNA (empty vector).

    Journal: International Journal of Molecular Sciences

    Article Title: p38 MAPK Is Activated but Does Not Play a Key Role during Apoptosis Induction by Saturated Fatty Acid in Human Pancreatic β-Cells

    doi: 10.3390/ijms17020159

    Figure Lengend Snippet: Effect of p38 MAPK overexpression, using transfection with a specific plasmid (Vector with p38 MAPK) (see “Materials and Methods”) and the effect of stearic acid (SA) on ( A ) the level of p38 MAPK, phospho-p38 MAPK and phospho-MAPKAPK-2 (substrate of p38 MAPK); ( B ) the level of phospho-c-Raf, phospho-MEK1/2, phospho-ERK1/2 (the ERK signaling pathway); and ( C ) cell growth and viability of NES2Y cells. Cells transfected with an empty vector (Empty vector) represented control cells. After 18 h of incubation (see “Materials and Methods”) with or without stearic acid (SA) ( A , B ), the level of individual proteins was determined using Western blot analysis and the relevant antibodies (see “Materials and Methods”). A monoclonal antibody against human actin was used to confirm equal protein loading. The data shown were obtained in one representative experiment from three independent experiments. The fact that the band of p38 MAPK in the control samples is not visible here resulted from a large difference in p38 MAPK content in control and transfected cells. When assessing cell growth and viability ( C ), cells were seeded at a concentration of 2 × 10 4 cells/100 µL of culture medium per well of 96-well plate (see “Materials and Methods”). The number of living cells was determined after 48 h of incubation with or without SA. Each column represents the mean of four separate cultures ± SEM. NS (non-significant) when comparing the number of cells incubated with plasmid DNA containing p38 MAPK (Vector with p38 MAPK) and cells incubated with empty plasmid DNA (empty vector).

    Article Snippet: The p38 MAPK inhibitor SB202190, the activator anisomycin, and SA were applied in the same way as described above (“Inhibitor and activator application”).

    Techniques: Over Expression, Transfection, Plasmid Preparation, Incubation, Western Blot, Concentration Assay

    Effect of 1 mM stearic acid (SA) (see “Materials and Methods”) on ( A ) cell growth and viability; ( B ) the level of cleaved PARP, caspase-7 (C7), caspase-8 (C8) and caspase-9 (C9) (markers of apoptosis); ( C ) the level of phospho-MKK3/6, p38 MAPK, phospho-p38 MAPK, phospho-MAPKAPK-2 (p38 MAPK signaling pathway); and ( D ) the level of phospho-c-Raf, phospho-MEK1/2, ERK1/2, phospho-ERK1/2 (the ERK signaling pathway) in NES2Y cells. Cells incubated without SA represented control cells. After 18 h of incubation (see “Materials and Methods”) for markers of apoptosis ( B ) and 3, 6, 12 and 24 h of incubation for p38 MAPK and ERK pathways members ( C , D ), the levels of individual proteins were determined using Western blot analysis and the relevant antibodies (see “Materials and Methods”). Monoclonal antibody against human actin was used to confirm equal protein loading. The data shown were obtained in one representative experiment from at least three independent experiments. When assessing cell growth and viability ( A ), cells were seeded at a concentration of 2 × 10 4 cells/100 µL of culture medium per well of 96-well plate (see “Materials and Methods”). The number of living cells was determined after 48 h of incubation. Each column represents the mean of four separate cultures ± standard error of the mean (SEM). * p

    Journal: International Journal of Molecular Sciences

    Article Title: p38 MAPK Is Activated but Does Not Play a Key Role during Apoptosis Induction by Saturated Fatty Acid in Human Pancreatic β-Cells

    doi: 10.3390/ijms17020159

    Figure Lengend Snippet: Effect of 1 mM stearic acid (SA) (see “Materials and Methods”) on ( A ) cell growth and viability; ( B ) the level of cleaved PARP, caspase-7 (C7), caspase-8 (C8) and caspase-9 (C9) (markers of apoptosis); ( C ) the level of phospho-MKK3/6, p38 MAPK, phospho-p38 MAPK, phospho-MAPKAPK-2 (p38 MAPK signaling pathway); and ( D ) the level of phospho-c-Raf, phospho-MEK1/2, ERK1/2, phospho-ERK1/2 (the ERK signaling pathway) in NES2Y cells. Cells incubated without SA represented control cells. After 18 h of incubation (see “Materials and Methods”) for markers of apoptosis ( B ) and 3, 6, 12 and 24 h of incubation for p38 MAPK and ERK pathways members ( C , D ), the levels of individual proteins were determined using Western blot analysis and the relevant antibodies (see “Materials and Methods”). Monoclonal antibody against human actin was used to confirm equal protein loading. The data shown were obtained in one representative experiment from at least three independent experiments. When assessing cell growth and viability ( A ), cells were seeded at a concentration of 2 × 10 4 cells/100 µL of culture medium per well of 96-well plate (see “Materials and Methods”). The number of living cells was determined after 48 h of incubation. Each column represents the mean of four separate cultures ± standard error of the mean (SEM). * p

    Article Snippet: The p38 MAPK inhibitor SB202190, the activator anisomycin, and SA were applied in the same way as described above (“Inhibitor and activator application”).

    Techniques: Incubation, Western Blot, Concentration Assay

    Effect of the specific p38 MAPK activator, anisomycin, (see “Materials and Methods”) and the effect of stearic acid (SA) on ( A ) the level of p38 MAPK, phospho-p38 MAPK and phospho-MAPKAPK-2 (substrate of p38 MAPK); ( B ) the level of phospho-c-Raf, phospho-MEK1/2, phospho-ERK1/2 (the ERK signaling pathway); ( C ) cell growth and viability; and ( D ) cleavage of PARP, caspase-7 (C7), caspase-8 (C8) and caspase-9 (C9) (markers of apoptosis) in NES2Y cells. Cells incubated without the activator and SA represented control cells. After 12 h of incubation (see “Materials and Methods”) ( A , B , D ), the level of individual proteins was determined using western blot analysis and the relevant antibodies (see “Materials and Methods”). A monoclonal antibody against human actin was used to confirm equal protein loading. The data shown were obtained in one representative experiment from three independent experiments. When assessing cell growth and viability ( C ), cells were seeded at a concentration of 2 × 10 4 cells/100 µL of culture medium per well of 96-well plate (see “Materials and Methods”). The number of living cells was determined after 48 h of incubation. Each column represents the mean of four separate cultures ± SEM. * p

    Journal: International Journal of Molecular Sciences

    Article Title: p38 MAPK Is Activated but Does Not Play a Key Role during Apoptosis Induction by Saturated Fatty Acid in Human Pancreatic β-Cells

    doi: 10.3390/ijms17020159

    Figure Lengend Snippet: Effect of the specific p38 MAPK activator, anisomycin, (see “Materials and Methods”) and the effect of stearic acid (SA) on ( A ) the level of p38 MAPK, phospho-p38 MAPK and phospho-MAPKAPK-2 (substrate of p38 MAPK); ( B ) the level of phospho-c-Raf, phospho-MEK1/2, phospho-ERK1/2 (the ERK signaling pathway); ( C ) cell growth and viability; and ( D ) cleavage of PARP, caspase-7 (C7), caspase-8 (C8) and caspase-9 (C9) (markers of apoptosis) in NES2Y cells. Cells incubated without the activator and SA represented control cells. After 12 h of incubation (see “Materials and Methods”) ( A , B , D ), the level of individual proteins was determined using western blot analysis and the relevant antibodies (see “Materials and Methods”). A monoclonal antibody against human actin was used to confirm equal protein loading. The data shown were obtained in one representative experiment from three independent experiments. When assessing cell growth and viability ( C ), cells were seeded at a concentration of 2 × 10 4 cells/100 µL of culture medium per well of 96-well plate (see “Materials and Methods”). The number of living cells was determined after 48 h of incubation. Each column represents the mean of four separate cultures ± SEM. * p

    Article Snippet: The p38 MAPK inhibitor SB202190, the activator anisomycin, and SA were applied in the same way as described above (“Inhibitor and activator application”).

    Techniques: Incubation, Western Blot, Concentration Assay

    Effect of the specific p38 MAPK inhibitor, SB202190, (see “Materials and Methods”) and the effect of stearic acid (SA) on ( A ) the level of phospho-MAPKAPK-2 (substrate of p38 MAPK); ( B ) the level of phospho-c-Raf, phospho-MEK1/2, phospho-ERK1/2 (the ERK signaling pathway); and ( C ) cell growth and viability of NES2Y cells. Cells incubated without the inhibitor represented control cells. After 12 h of incubation (see “Materials and Methods”) ( A , B ), the level of individual proteins was determined using Western blot analysis and the relevant antibodies (see “Materials and Methods”). A monoclonal antibody against human actin was used to confirm equal protein loading. The data shown were obtained in one representative experiment from three independent experiments. When assessing cell growth and viability ( C ), cells were seeded at a concentration of 2 × 10 4 cells/100 µL of culture medium per well of 96-well plate (see “Materials and Methods”). The number of living cells was determined after 48 h of incubation. Each column represents the mean of four separate cultures ± SEM. NS (non-significant) when comparing the number of control cells and cells treated with SB202190 as well as when comparing the effect of SA alone and applied together with SB202190.

    Journal: International Journal of Molecular Sciences

    Article Title: p38 MAPK Is Activated but Does Not Play a Key Role during Apoptosis Induction by Saturated Fatty Acid in Human Pancreatic β-Cells

    doi: 10.3390/ijms17020159

    Figure Lengend Snippet: Effect of the specific p38 MAPK inhibitor, SB202190, (see “Materials and Methods”) and the effect of stearic acid (SA) on ( A ) the level of phospho-MAPKAPK-2 (substrate of p38 MAPK); ( B ) the level of phospho-c-Raf, phospho-MEK1/2, phospho-ERK1/2 (the ERK signaling pathway); and ( C ) cell growth and viability of NES2Y cells. Cells incubated without the inhibitor represented control cells. After 12 h of incubation (see “Materials and Methods”) ( A , B ), the level of individual proteins was determined using Western blot analysis and the relevant antibodies (see “Materials and Methods”). A monoclonal antibody against human actin was used to confirm equal protein loading. The data shown were obtained in one representative experiment from three independent experiments. When assessing cell growth and viability ( C ), cells were seeded at a concentration of 2 × 10 4 cells/100 µL of culture medium per well of 96-well plate (see “Materials and Methods”). The number of living cells was determined after 48 h of incubation. Each column represents the mean of four separate cultures ± SEM. NS (non-significant) when comparing the number of control cells and cells treated with SB202190 as well as when comparing the effect of SA alone and applied together with SB202190.

    Article Snippet: The p38 MAPK inhibitor SB202190, the activator anisomycin, and SA were applied in the same way as described above (“Inhibitor and activator application”).

    Techniques: Incubation, Western Blot, Concentration Assay

    Phospho-p38 MAPK inhibitors prevent and reverse EndoMT-associated gene expression in vitro. ( a ) To study possible prevention of EndoMT, hREC were treated with the p38 MAPK inhibitor SB203580 or SB202190 (10 μM) during EndoMT induction. Expression levels for the genes encoding the EndoMT-associated proteins SNAI1, SNAI2, α-SMA, FSP-1, vimentin, fibronectin, COL1A2 and COL3A1; and the endothelial differentiation markers VE-cadherin, CD31 and VEGFR2 were assessed by qPCR on day 6 of EndoMT induction. Data = mean ± SEM, * p

    Journal: Cells

    Article Title: Fibrotic Changes and Endothelial-to-Mesenchymal Transition Promoted by VEGFR2 Antagonism Alter the Therapeutic Effects of VEGFA Pathway Blockage in a Mouse Model of Choroidal Neovascularization

    doi: 10.3390/cells9092057

    Figure Lengend Snippet: Phospho-p38 MAPK inhibitors prevent and reverse EndoMT-associated gene expression in vitro. ( a ) To study possible prevention of EndoMT, hREC were treated with the p38 MAPK inhibitor SB203580 or SB202190 (10 μM) during EndoMT induction. Expression levels for the genes encoding the EndoMT-associated proteins SNAI1, SNAI2, α-SMA, FSP-1, vimentin, fibronectin, COL1A2 and COL3A1; and the endothelial differentiation markers VE-cadherin, CD31 and VEGFR2 were assessed by qPCR on day 6 of EndoMT induction. Data = mean ± SEM, * p

    Article Snippet: For the prevention study using the p38 MAPK inhibitors, SB203580 or SB202190 (10 μM, Abcam, Cambridge, MA, USA) was applied with the pro-inflammatory cytokines at the beginning of induction and again at day three; expression of endothelial and EndoMT markers was analyzed by RT-qPCR at day six.

    Techniques: Expressing, In Vitro, Real-time Polymerase Chain Reaction