sb202190  (InvivoGen)

 
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    Name:
    SB202190
    Description:
    MAP Kinase Inhibitor
    Catalog Number:
    tlrl-sb90
    Price:
    None
    Category:
    SB202190 NF κB MAPK Activation Inhibitors Immunomodulators Inhibitors
    Size:
    5 mg
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    Structured Review

    InvivoGen sb202190
    ALS induces autophagy via PI3K-mediated and p38 MAPK-mediated signaling pathways in AGS and NCI-N78 cells. Notes: AGS and NCI-N78 cells were pretreated with <t>SB202190</t> or wortmannin for 1 hour and then incubated for another 24 hours in the presence or absence of 1 μM ALS. ( A ) Representative images show autophagy of AGS and NCI-N78 cells. ( B ) Bar graphs show the percentage of autophagic AGS and NCI-N78 cells. Data are the mean ± SD of three independent experiments. * P
    MAP Kinase Inhibitor
    https://www.bioz.com/result/sb202190/product/InvivoGen
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    sb202190 - by Bioz Stars, 2021-03
    86/100 stars

    Images

    1) Product Images from "Inhibition of mitotic Aurora kinase A by alisertib induces apoptosis and autophagy of human gastric cancer AGS and NCI-N78 cells"

    Article Title: Inhibition of mitotic Aurora kinase A by alisertib induces apoptosis and autophagy of human gastric cancer AGS and NCI-N78 cells

    Journal: Drug Design, Development and Therapy

    doi: 10.2147/DDDT.S74127

    ALS induces autophagy via PI3K-mediated and p38 MAPK-mediated signaling pathways in AGS and NCI-N78 cells. Notes: AGS and NCI-N78 cells were pretreated with SB202190 or wortmannin for 1 hour and then incubated for another 24 hours in the presence or absence of 1 μM ALS. ( A ) Representative images show autophagy of AGS and NCI-N78 cells. ( B ) Bar graphs show the percentage of autophagic AGS and NCI-N78 cells. Data are the mean ± SD of three independent experiments. * P
    Figure Legend Snippet: ALS induces autophagy via PI3K-mediated and p38 MAPK-mediated signaling pathways in AGS and NCI-N78 cells. Notes: AGS and NCI-N78 cells were pretreated with SB202190 or wortmannin for 1 hour and then incubated for another 24 hours in the presence or absence of 1 μM ALS. ( A ) Representative images show autophagy of AGS and NCI-N78 cells. ( B ) Bar graphs show the percentage of autophagic AGS and NCI-N78 cells. Data are the mean ± SD of three independent experiments. * P

    Techniques Used: Incubation

    2) Product Images from "Alisertib promotes apoptosis and autophagy in melanoma through p38 MAPK-mediated aurora a signaling"

    Article Title: Alisertib promotes apoptosis and autophagy in melanoma through p38 MAPK-mediated aurora a signaling

    Journal: Oncotarget

    doi: 10.18632/oncotarget.22328

    SB202190 enhances ALS-induced apoptosis and autophagy in A375 and skmel-5 cells (A) Flow cytometry analysis of apoptosis in A375 and skmel-5 cells after treatment with ALS, SB202190, or SB202190 + ALS for 24 hours; (B) Flow cytometry analysis of autophagy in A375 and skmel-5 cells after treatment with ALS, SB202190, or SB202190 + ALS for 24 hours; (C) Quantification of apoptotic A375 and skmel-5 cells after treatment with ALS, SB202190, or SB202190 + ALS; (D) Quantification of autophagic A375 and skmel-5 cells after treatment with ALS, SB202190, or SB202190 + ALS; (E) Western blot analysis of the levels of p38 MAPK signaling pathway components in A375 and skmel-5 cells after treatment with ALS, SB202190, or SB202190 + ALS; (F) Quantification of relative protein levels. Data are expressed as the means ± SD. All experiments were repeated at least three times. ( * p
    Figure Legend Snippet: SB202190 enhances ALS-induced apoptosis and autophagy in A375 and skmel-5 cells (A) Flow cytometry analysis of apoptosis in A375 and skmel-5 cells after treatment with ALS, SB202190, or SB202190 + ALS for 24 hours; (B) Flow cytometry analysis of autophagy in A375 and skmel-5 cells after treatment with ALS, SB202190, or SB202190 + ALS for 24 hours; (C) Quantification of apoptotic A375 and skmel-5 cells after treatment with ALS, SB202190, or SB202190 + ALS; (D) Quantification of autophagic A375 and skmel-5 cells after treatment with ALS, SB202190, or SB202190 + ALS; (E) Western blot analysis of the levels of p38 MAPK signaling pathway components in A375 and skmel-5 cells after treatment with ALS, SB202190, or SB202190 + ALS; (F) Quantification of relative protein levels. Data are expressed as the means ± SD. All experiments were repeated at least three times. ( * p

    Techniques Used: Flow Cytometry, Cytometry, Western Blot

    ALS induces cell cycle arrest in A375 and skmel-5 cells (A) Flow cytometry analysis of the cell cycle distribution of A375 and skmel-5 cells following treatment with ALS at concentrations ranging from 0 to 5 μM for 24 hours; (B) Quantification of A375 and skmel-5 cells in G2/M phase and aneuploid cells after treatment with ALS; (C) Western blot analysis of the levels of p53/p21/cyclin B1 pathway components in A375 and skmel-5 cells after treatment with ALS at concentrations ranging from 0 to 5 μM; (D) Western blot analysis of the levels of p53/p21/cyclin B1 pathway components in A375 and skmel-5 cells after treatment with ALS, SB202190, or SB202190 + ALS; (E) Quantification of the relative protein levels. Data are expressed as the means ± SD. All experiments were repeated at least three times. ( * p
    Figure Legend Snippet: ALS induces cell cycle arrest in A375 and skmel-5 cells (A) Flow cytometry analysis of the cell cycle distribution of A375 and skmel-5 cells following treatment with ALS at concentrations ranging from 0 to 5 μM for 24 hours; (B) Quantification of A375 and skmel-5 cells in G2/M phase and aneuploid cells after treatment with ALS; (C) Western blot analysis of the levels of p53/p21/cyclin B1 pathway components in A375 and skmel-5 cells after treatment with ALS at concentrations ranging from 0 to 5 μM; (D) Western blot analysis of the levels of p53/p21/cyclin B1 pathway components in A375 and skmel-5 cells after treatment with ALS, SB202190, or SB202190 + ALS; (E) Quantification of the relative protein levels. Data are expressed as the means ± SD. All experiments were repeated at least three times. ( * p

    Techniques Used: Flow Cytometry, Cytometry, Western Blot

    3) Product Images from "The pan-inhibitor of Aurora kinases danusertib induces apoptosis and autophagy and suppresses epithelial-to-mesenchymal transition in human breast cancer cells"

    Article Title: The pan-inhibitor of Aurora kinases danusertib induces apoptosis and autophagy and suppresses epithelial-to-mesenchymal transition in human breast cancer cells

    Journal: Drug Design, Development and Therapy

    doi: 10.2147/DDDT.S74412

    Effects of specific p38 MAPK and Erk1/2 inhibitors on Danu-induced autophagy in MCF7 cells and MDA-MB-231 cells. Notes: Cells were pretreated with SB202190 (10 μM) or U0126 (10 μM) for 30 minutes, 0.5 μM Danu was added for further incubation of 24 hours, and cells were harvested. The percentage of autophagic MCF7 and MDA-MB-231 cells was examined by flow cytometry with Cyto-ID ® as the green stain for autophagic vacuoles. ( A ) Flow cytometric dot plots showing the autophagic MCF7 and MDA-MB-23 cells, and ( B ) bar graphs showing the percentage of autophagic MCF7 and MDA-MB-231 cells. Data are expressed as the mean ± SD of three independent experiments. * P
    Figure Legend Snippet: Effects of specific p38 MAPK and Erk1/2 inhibitors on Danu-induced autophagy in MCF7 cells and MDA-MB-231 cells. Notes: Cells were pretreated with SB202190 (10 μM) or U0126 (10 μM) for 30 minutes, 0.5 μM Danu was added for further incubation of 24 hours, and cells were harvested. The percentage of autophagic MCF7 and MDA-MB-231 cells was examined by flow cytometry with Cyto-ID ® as the green stain for autophagic vacuoles. ( A ) Flow cytometric dot plots showing the autophagic MCF7 and MDA-MB-23 cells, and ( B ) bar graphs showing the percentage of autophagic MCF7 and MDA-MB-231 cells. Data are expressed as the mean ± SD of three independent experiments. * P

    Techniques Used: Multiple Displacement Amplification, Incubation, Flow Cytometry, Cytometry, Staining

    Effects of various chemical modulators on the expression levels of beclin 1 and LC3-II in MCF7 cells and MDA-MB-231 cells. Notes: Cells were pretreated with WM (10 μM), bafilomycin A1 (100 nM), SB202190 (10 μM), or U0126 (10 μM) for 30 minutes, 0.5 μM Danu was added and incubated for a further 24 hours, cells were harvested, and protein samples were subjected to Western blotting assay. ( A ) Representative blots of beclin 1 and LC3-II in MCF7 cells and MDA-MB-231 cells, and ( B ) bar graphs showing the relative levels of beclin 1 and LC3-II. β-actin was used as the internal control. Data are expressed as the mean ± SD of three independent experiments. * P
    Figure Legend Snippet: Effects of various chemical modulators on the expression levels of beclin 1 and LC3-II in MCF7 cells and MDA-MB-231 cells. Notes: Cells were pretreated with WM (10 μM), bafilomycin A1 (100 nM), SB202190 (10 μM), or U0126 (10 μM) for 30 minutes, 0.5 μM Danu was added and incubated for a further 24 hours, cells were harvested, and protein samples were subjected to Western blotting assay. ( A ) Representative blots of beclin 1 and LC3-II in MCF7 cells and MDA-MB-231 cells, and ( B ) bar graphs showing the relative levels of beclin 1 and LC3-II. β-actin was used as the internal control. Data are expressed as the mean ± SD of three independent experiments. * P

    Techniques Used: Expressing, Multiple Displacement Amplification, Incubation, Western Blot

    4) Product Images from "miR-625-3p regulates oxaliplatin resistance by targeting MAP2K6-p38 signalling in human colorectal adenocarcinoma cells"

    Article Title: miR-625-3p regulates oxaliplatin resistance by targeting MAP2K6-p38 signalling in human colorectal adenocarcinoma cells

    Journal: Nature Communications

    doi: 10.1038/ncomms12436

    Inhibition of MAPK14 induces oxaliplatin resistance in CRC cells. ( a ) MAPK14 was specifically depleted from HCT116 and SW620 cells by transfection of a pool of MAPK14 targeting siRNAs (siR MAPK14 ) 48 h before being treated with 64 μM oxPt for 48 h (or left unexposed; see Supplementary Fig. 9 for knockdown efficiencies). The impact on cell death (64 μM/0 μM) was determined by LDH and are displayed relative to cells transfected with a scrambled siRNA (siR scr , set to 1). Mean±s.e.m. from at least n =4 experiments with ‘*' indicating a significant reduction in oxPt-induced cells death compared with siR scr transfected cells ( P ≤0.05, t -test). ( b ) A phospho-specific western blot versus the MAPK14/MAPKAPK2 substrate Ser82-HSPB1 was applied to show increased MAPK14 activity after oxPt treatment and the inhibitory effect of 10 μM SB203580 on this activity. ( c ) HCT116 and SW620 cells were treated for 1 h with MAPK11/14 inhibitors SB203580 (10 μM, blue) or SB202190 (5 μM, purple), then exposed to 64 μM oxPt (or left unexposed) for 48 h before the increase in cell death (64 μM/0 μM) was determined by LDH. Presented relative to cells not treated with inhibitor (DMSO treated; mean±s.e.m. from at least n =4 experiments with ‘*' indicating a significant reduction in oxPt-induced death compared with DMSO-treated cells, P ≤0.05, t -test). ( d ) Stable, inducible expression of miR-625-3p was generated using pSBInducer transposition in HCC2998 CRC cells (left). Phospho-specific western blot for MAP2K6 and MAPK14 activity 48 h after DOX induction of HCC2998.ctrl and HCC2998.625 cells (right). ( e ) HCC2298.ctrl and HCC2998.625 cells DOX-induced for 48 h, then treated (or left untreated) with 64 μM oxPt for 48 h before the increase in cell death (64 μM/0 μM) was determined by LDH. Results are displayed relative to control cells (set to 1; mean±s.e.m. from n =3 experiments; * P ≤0.05, t -test). ( f , g ) HCC2998, Colo205, DLD1, HT29 and LoVo CRC cells were treated for 1 h with MAPK11/14 inhibitors SB203580 (10 μM, blue) or SB202190 (5 μM, purple) then exposed to 64 μM oxPt (or left unexposed) for 48 h before the increase in cell death (64 μM/0 μM) was determined by LDH. Displayed relative to DMSO-treated cells (mean±s.e.m. from n =3–4 experiments with ‘*' indicating a significant reduction, P ≤0.05, t -test). ( h ) A schematic model showing how miR-625-3p mediated downregulation of MAP2K6 could modulate response to oxPt by abrogating MAPK14 stress-induced signalling. In the canonical model MAP2K6 in complex with MAP2K3 phosphorylates and activates MAPK14, which in turn—directly or indirectly via substrate kinases such as MAPKAPK2—activates a diverse number of target proteins central to stress-induced transcription, translation, cell cycle control and apoptosis.
    Figure Legend Snippet: Inhibition of MAPK14 induces oxaliplatin resistance in CRC cells. ( a ) MAPK14 was specifically depleted from HCT116 and SW620 cells by transfection of a pool of MAPK14 targeting siRNAs (siR MAPK14 ) 48 h before being treated with 64 μM oxPt for 48 h (or left unexposed; see Supplementary Fig. 9 for knockdown efficiencies). The impact on cell death (64 μM/0 μM) was determined by LDH and are displayed relative to cells transfected with a scrambled siRNA (siR scr , set to 1). Mean±s.e.m. from at least n =4 experiments with ‘*' indicating a significant reduction in oxPt-induced cells death compared with siR scr transfected cells ( P ≤0.05, t -test). ( b ) A phospho-specific western blot versus the MAPK14/MAPKAPK2 substrate Ser82-HSPB1 was applied to show increased MAPK14 activity after oxPt treatment and the inhibitory effect of 10 μM SB203580 on this activity. ( c ) HCT116 and SW620 cells were treated for 1 h with MAPK11/14 inhibitors SB203580 (10 μM, blue) or SB202190 (5 μM, purple), then exposed to 64 μM oxPt (or left unexposed) for 48 h before the increase in cell death (64 μM/0 μM) was determined by LDH. Presented relative to cells not treated with inhibitor (DMSO treated; mean±s.e.m. from at least n =4 experiments with ‘*' indicating a significant reduction in oxPt-induced death compared with DMSO-treated cells, P ≤0.05, t -test). ( d ) Stable, inducible expression of miR-625-3p was generated using pSBInducer transposition in HCC2998 CRC cells (left). Phospho-specific western blot for MAP2K6 and MAPK14 activity 48 h after DOX induction of HCC2998.ctrl and HCC2998.625 cells (right). ( e ) HCC2298.ctrl and HCC2998.625 cells DOX-induced for 48 h, then treated (or left untreated) with 64 μM oxPt for 48 h before the increase in cell death (64 μM/0 μM) was determined by LDH. Results are displayed relative to control cells (set to 1; mean±s.e.m. from n =3 experiments; * P ≤0.05, t -test). ( f , g ) HCC2998, Colo205, DLD1, HT29 and LoVo CRC cells were treated for 1 h with MAPK11/14 inhibitors SB203580 (10 μM, blue) or SB202190 (5 μM, purple) then exposed to 64 μM oxPt (or left unexposed) for 48 h before the increase in cell death (64 μM/0 μM) was determined by LDH. Displayed relative to DMSO-treated cells (mean±s.e.m. from n =3–4 experiments with ‘*' indicating a significant reduction, P ≤0.05, t -test). ( h ) A schematic model showing how miR-625-3p mediated downregulation of MAP2K6 could modulate response to oxPt by abrogating MAPK14 stress-induced signalling. In the canonical model MAP2K6 in complex with MAP2K3 phosphorylates and activates MAPK14, which in turn—directly or indirectly via substrate kinases such as MAPKAPK2—activates a diverse number of target proteins central to stress-induced transcription, translation, cell cycle control and apoptosis.

    Techniques Used: Inhibition, Transfection, Western Blot, Activity Assay, Expressing, Generated

    5) Product Images from "Danusertib, a potent pan-Aurora kinase and ABL kinase inhibitor, induces cell cycle arrest and programmed cell death and inhibits epithelial to mesenchymal transition involving the PI3K/Akt/mTOR-mediated signaling pathway in human gastric cancer AGS and NCI-N78 cells"

    Article Title: Danusertib, a potent pan-Aurora kinase and ABL kinase inhibitor, induces cell cycle arrest and programmed cell death and inhibits epithelial to mesenchymal transition involving the PI3K/Akt/mTOR-mediated signaling pathway in human gastric cancer AGS and NCI-N78 cells

    Journal: Drug Design, Development and Therapy

    doi: 10.2147/DDDT.S74964

    Danusertib induces autophagy via PI3K-mediated and p38 MAPK-mediated signaling pathways determined by flow cytometry. Notes: AGS and NCI-N78 cells were pretreated with SB202190 and WM for one hour and then incubated with danusertib for another 24 hours in the presence or absence of 0.5 μM danusertib. The cell samples were subjected to flow cytometry. ( A ) Flow cytometric plots showing autophagy of AGS and NCI-N78 cells and ( B ) bar graphs showing the percentage of autophagic AGS and NCI-N78 cells. Data represent the mean ± standard deviation of three independent experiments. ** P
    Figure Legend Snippet: Danusertib induces autophagy via PI3K-mediated and p38 MAPK-mediated signaling pathways determined by flow cytometry. Notes: AGS and NCI-N78 cells were pretreated with SB202190 and WM for one hour and then incubated with danusertib for another 24 hours in the presence or absence of 0.5 μM danusertib. The cell samples were subjected to flow cytometry. ( A ) Flow cytometric plots showing autophagy of AGS and NCI-N78 cells and ( B ) bar graphs showing the percentage of autophagic AGS and NCI-N78 cells. Data represent the mean ± standard deviation of three independent experiments. ** P

    Techniques Used: Flow Cytometry, Cytometry, Incubation, Standard Deviation

    Danusertib induces autophagy via PI3K-mediated and p38 MAPK-mediated signaling determined by confocal microscopy. Notes: AGS and NCI-N78 cells were pretreated with SB202190 and WM for one hour and then incubated for another 24 hours in the presence or absence of 0.5 μM danusertib. The cell samples were subjected to confocal microscopy. ( A ) Representative images showing autophagy of AGS and NCI-N78 cells and ( B ) bar graphs showing the percentage of autophagic AGS and NCI-N78 cells. Data represent the mean ± standard deviation of three independent experiments. Magnification 60×; scale bar 5 μM. * P
    Figure Legend Snippet: Danusertib induces autophagy via PI3K-mediated and p38 MAPK-mediated signaling determined by confocal microscopy. Notes: AGS and NCI-N78 cells were pretreated with SB202190 and WM for one hour and then incubated for another 24 hours in the presence or absence of 0.5 μM danusertib. The cell samples were subjected to confocal microscopy. ( A ) Representative images showing autophagy of AGS and NCI-N78 cells and ( B ) bar graphs showing the percentage of autophagic AGS and NCI-N78 cells. Data represent the mean ± standard deviation of three independent experiments. Magnification 60×; scale bar 5 μM. * P

    Techniques Used: Confocal Microscopy, Incubation, Standard Deviation

    6) Product Images from "Plumbagin induces cell cycle arrest and autophagy and suppresses epithelial to mesenchymal transition involving PI3K/Akt/mTOR-mediated pathway in human pancreatic cancer cells"

    Article Title: Plumbagin induces cell cycle arrest and autophagy and suppresses epithelial to mesenchymal transition involving PI3K/Akt/mTOR-mediated pathway in human pancreatic cancer cells

    Journal: Drug Design, Development and Therapy

    doi: 10.2147/DDDT.S73689

    PLB regulates autophagy via p38 MAPK and PI3K/Akt signaling pathways in PANC-1 and BxPC-3 cells. Notes: Cells were pretreated with 10 μM SB202190 or 10 μM WM for 1 hour and then incubated with or without 5 μM PLB for another 24 hours. ( A ) Flow cytometric plots of PANC-1 cells; ( B ) flow cytometric plots of BxPC-3 cells; ( C ) bar graphs showing percentage of autophagic cells in PANC-1 and BxPC-3 cells. Data represent the mean ± SD. * P
    Figure Legend Snippet: PLB regulates autophagy via p38 MAPK and PI3K/Akt signaling pathways in PANC-1 and BxPC-3 cells. Notes: Cells were pretreated with 10 μM SB202190 or 10 μM WM for 1 hour and then incubated with or without 5 μM PLB for another 24 hours. ( A ) Flow cytometric plots of PANC-1 cells; ( B ) flow cytometric plots of BxPC-3 cells; ( C ) bar graphs showing percentage of autophagic cells in PANC-1 and BxPC-3 cells. Data represent the mean ± SD. * P

    Techniques Used: Incubation, Flow Cytometry

    7) Product Images from "MAPK Activation Is Essential for Waddlia chondrophila Induced CXCL8 Expression in Human Epithelial Cells"

    Article Title: MAPK Activation Is Essential for Waddlia chondrophila Induced CXCL8 Expression in Human Epithelial Cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0152193

    The effects of MAPK inhibitors upon W . chondrophila replication and CXCL8 secretion in HEp2 cells. Cells were pre-treated for 2h prior to infection with W . chondrophila (MOI 10). A) Western blot demonstrating induction of p42/44 and p38 MAPK by W . chondrophila and inhibition by the specific inhibitors UO126 (p42/44 MAPK) and SB202190 (p38 MAPK). As a positive control for both p42/44 and p38 phosphorylation cells were exposed to EGF for 5 mins. B) and C) The effects of increasing concentrations of the p42/44 MAPK inhibitor UO126 on bacterial replication and CXCL8 release respectively. Statistically-significant reductions in CXCL8 relative to infected vehicle control cells are indicated by ***P
    Figure Legend Snippet: The effects of MAPK inhibitors upon W . chondrophila replication and CXCL8 secretion in HEp2 cells. Cells were pre-treated for 2h prior to infection with W . chondrophila (MOI 10). A) Western blot demonstrating induction of p42/44 and p38 MAPK by W . chondrophila and inhibition by the specific inhibitors UO126 (p42/44 MAPK) and SB202190 (p38 MAPK). As a positive control for both p42/44 and p38 phosphorylation cells were exposed to EGF for 5 mins. B) and C) The effects of increasing concentrations of the p42/44 MAPK inhibitor UO126 on bacterial replication and CXCL8 release respectively. Statistically-significant reductions in CXCL8 relative to infected vehicle control cells are indicated by ***P

    Techniques Used: Infection, Western Blot, Inhibition, Positive Control

    8) Product Images from "The Complement Anaphylatoxins, C5a and C3a, Suppress Interferon-Beta Production in Response to Listeria monocytogenes by Inhibition of the Cyclic Dinucleotide-Activated Cytosolic Surveillance Pathway"

    Article Title: The Complement Anaphylatoxins, C5a and C3a, Suppress Interferon-Beta Production in Response to Listeria monocytogenes by Inhibition of the Cyclic Dinucleotide-Activated Cytosolic Surveillance Pathway

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1601420

    BTK, TBK1, and p38 MAPK are necessary for C5aA and C3aA to suppress IFN-β production WT BMDCs were pre-treated with either vehicle, (A) 100 nM CGI-1746 to inhibit BTK, (B) 10 μM U0126 to inhibit Erk, 0.25 μM Wortmannin to inhibit PI3K/Akt, (C) 10 nM BX795 to inhibit TBK1, or (D) 1 μM SB202190 to inhibit p38 MAPK. After 1 h, the cells were treated with either media, 100 nM C5aA, or 100 nM C3aA for 2 h followed by incubation with 25 μg/ml c-di-AMP for 20 h. IFN-β was quantitated from cell-free supernatants. All data are presented as mean pg/ml ± SEM. These data are pooled from three independent experiments. * P
    Figure Legend Snippet: BTK, TBK1, and p38 MAPK are necessary for C5aA and C3aA to suppress IFN-β production WT BMDCs were pre-treated with either vehicle, (A) 100 nM CGI-1746 to inhibit BTK, (B) 10 μM U0126 to inhibit Erk, 0.25 μM Wortmannin to inhibit PI3K/Akt, (C) 10 nM BX795 to inhibit TBK1, or (D) 1 μM SB202190 to inhibit p38 MAPK. After 1 h, the cells were treated with either media, 100 nM C5aA, or 100 nM C3aA for 2 h followed by incubation with 25 μg/ml c-di-AMP for 20 h. IFN-β was quantitated from cell-free supernatants. All data are presented as mean pg/ml ± SEM. These data are pooled from three independent experiments. * P

    Techniques Used: Incubation

    Related Articles

    Negative Control:

    Article Title: IL-32γ Delays Spontaneous Apoptosis of Human Neutrophils through MCL-1, Regulated Primarily by the p38 MAPK Pathway
    Article Snippet: The inhibitors of PI3K/Akt (LY294002) and MEK-1 (U0126) were obtained from Cayman Chemical (Ann Arbor, Michigan, USA). .. The JNK inhibitor (SP600125) was from Calbiochem (San Diego, CA, USA), p38 MAPK inhibitor (SB202190) was obtained from Invivogen (San Diego, CA, USA), and MAPK inhibitor negative control (SB202474) was from Life Technologies (Carlsbad, CA, USA). .. The fluorescein active caspase-3 staining kit was purchased from BioVision (Milpitas, CA, USA) and the caspase-3 (active form) apoptosis kit was from BD Biosciences (San Jose, CA, USA).

    Synthesized:

    Article Title: The Complement Anaphylatoxins, C5a and C3a, Suppress Interferon-Beta Production in Response to Listeria monocytogenes by Inhibition of the Cyclic Dinucleotide-Activated Cytosolic Surveillance Pathway
    Article Snippet: .. The C5aR agonist (C5aA) (RAARISLGPRSIKAFTE) ( ) and C3aR agonist (C3aA) (WWTRRWRGDKLGLAR) ( ) were synthesized by GenScript with greater than 95% purity. c-di-AMP, BX795, Wortmannin, U0126, and SB202190 were purchased from Invivogen. .. LPS from E. coli was purchased from List Labs, and CGI-1746 was purchased from ApexBio.

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    • p38 mapk inhibitor  (InvivoGen)
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    InvivoGen p38 mapk inhibitor
    IL-32γ induces phosphorylation of <t>p38</t> <t>MAPK</t> in human blood neutrophils. Freshly isolated neutrophils were incubated in the presence of IL-32γ (500 ng.ml −1 ) or its vehicle (HBSS) for the indicated time. Phosphorylation of p38 and total p38 were detected by immunoblot. Representative of 4 different donors.
    P38 Mapk Inhibitor, supplied by InvivoGen, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p38 mapk inhibitor/product/InvivoGen
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    IL-32γ induces phosphorylation of p38 MAPK in human blood neutrophils. Freshly isolated neutrophils were incubated in the presence of IL-32γ (500 ng.ml −1 ) or its vehicle (HBSS) for the indicated time. Phosphorylation of p38 and total p38 were detected by immunoblot. Representative of 4 different donors.

    Journal: PLoS ONE

    Article Title: IL-32γ Delays Spontaneous Apoptosis of Human Neutrophils through MCL-1, Regulated Primarily by the p38 MAPK Pathway

    doi: 10.1371/journal.pone.0109256

    Figure Lengend Snippet: IL-32γ induces phosphorylation of p38 MAPK in human blood neutrophils. Freshly isolated neutrophils were incubated in the presence of IL-32γ (500 ng.ml −1 ) or its vehicle (HBSS) for the indicated time. Phosphorylation of p38 and total p38 were detected by immunoblot. Representative of 4 different donors.

    Article Snippet: The JNK inhibitor (SP600125) was from Calbiochem (San Diego, CA, USA), p38 MAPK inhibitor (SB202190) was obtained from Invivogen (San Diego, CA, USA), and MAPK inhibitor negative control (SB202474) was from Life Technologies (Carlsbad, CA, USA).

    Techniques: Isolation, Incubation

    Inhibition of MAPK14 induces oxaliplatin resistance in CRC cells. ( a ) MAPK14 was specifically depleted from HCT116 and SW620 cells by transfection of a pool of MAPK14 targeting siRNAs (siR MAPK14 ) 48 h before being treated with 64 μM oxPt for 48 h (or left unexposed; see Supplementary Fig. 9 for knockdown efficiencies). The impact on cell death (64 μM/0 μM) was determined by LDH and are displayed relative to cells transfected with a scrambled siRNA (siR scr , set to 1). Mean±s.e.m. from at least n =4 experiments with ‘*' indicating a significant reduction in oxPt-induced cells death compared with siR scr transfected cells ( P ≤0.05, t -test). ( b ) A phospho-specific western blot versus the MAPK14/MAPKAPK2 substrate Ser82-HSPB1 was applied to show increased MAPK14 activity after oxPt treatment and the inhibitory effect of 10 μM SB203580 on this activity. ( c ) HCT116 and SW620 cells were treated for 1 h with MAPK11/14 inhibitors SB203580 (10 μM, blue) or SB202190 (5 μM, purple), then exposed to 64 μM oxPt (or left unexposed) for 48 h before the increase in cell death (64 μM/0 μM) was determined by LDH. Presented relative to cells not treated with inhibitor (DMSO treated; mean±s.e.m. from at least n =4 experiments with ‘*' indicating a significant reduction in oxPt-induced death compared with DMSO-treated cells, P ≤0.05, t -test). ( d ) Stable, inducible expression of miR-625-3p was generated using pSBInducer transposition in HCC2998 CRC cells (left). Phospho-specific western blot for MAP2K6 and MAPK14 activity 48 h after DOX induction of HCC2998.ctrl and HCC2998.625 cells (right). ( e ) HCC2298.ctrl and HCC2998.625 cells DOX-induced for 48 h, then treated (or left untreated) with 64 μM oxPt for 48 h before the increase in cell death (64 μM/0 μM) was determined by LDH. Results are displayed relative to control cells (set to 1; mean±s.e.m. from n =3 experiments; * P ≤0.05, t -test). ( f , g ) HCC2998, Colo205, DLD1, HT29 and LoVo CRC cells were treated for 1 h with MAPK11/14 inhibitors SB203580 (10 μM, blue) or SB202190 (5 μM, purple) then exposed to 64 μM oxPt (or left unexposed) for 48 h before the increase in cell death (64 μM/0 μM) was determined by LDH. Displayed relative to DMSO-treated cells (mean±s.e.m. from n =3–4 experiments with ‘*' indicating a significant reduction, P ≤0.05, t -test). ( h ) A schematic model showing how miR-625-3p mediated downregulation of MAP2K6 could modulate response to oxPt by abrogating MAPK14 stress-induced signalling. In the canonical model MAP2K6 in complex with MAP2K3 phosphorylates and activates MAPK14, which in turn—directly or indirectly via substrate kinases such as MAPKAPK2—activates a diverse number of target proteins central to stress-induced transcription, translation, cell cycle control and apoptosis.

    Journal: Nature Communications

    Article Title: miR-625-3p regulates oxaliplatin resistance by targeting MAP2K6-p38 signalling in human colorectal adenocarcinoma cells

    doi: 10.1038/ncomms12436

    Figure Lengend Snippet: Inhibition of MAPK14 induces oxaliplatin resistance in CRC cells. ( a ) MAPK14 was specifically depleted from HCT116 and SW620 cells by transfection of a pool of MAPK14 targeting siRNAs (siR MAPK14 ) 48 h before being treated with 64 μM oxPt for 48 h (or left unexposed; see Supplementary Fig. 9 for knockdown efficiencies). The impact on cell death (64 μM/0 μM) was determined by LDH and are displayed relative to cells transfected with a scrambled siRNA (siR scr , set to 1). Mean±s.e.m. from at least n =4 experiments with ‘*' indicating a significant reduction in oxPt-induced cells death compared with siR scr transfected cells ( P ≤0.05, t -test). ( b ) A phospho-specific western blot versus the MAPK14/MAPKAPK2 substrate Ser82-HSPB1 was applied to show increased MAPK14 activity after oxPt treatment and the inhibitory effect of 10 μM SB203580 on this activity. ( c ) HCT116 and SW620 cells were treated for 1 h with MAPK11/14 inhibitors SB203580 (10 μM, blue) or SB202190 (5 μM, purple), then exposed to 64 μM oxPt (or left unexposed) for 48 h before the increase in cell death (64 μM/0 μM) was determined by LDH. Presented relative to cells not treated with inhibitor (DMSO treated; mean±s.e.m. from at least n =4 experiments with ‘*' indicating a significant reduction in oxPt-induced death compared with DMSO-treated cells, P ≤0.05, t -test). ( d ) Stable, inducible expression of miR-625-3p was generated using pSBInducer transposition in HCC2998 CRC cells (left). Phospho-specific western blot for MAP2K6 and MAPK14 activity 48 h after DOX induction of HCC2998.ctrl and HCC2998.625 cells (right). ( e ) HCC2298.ctrl and HCC2998.625 cells DOX-induced for 48 h, then treated (or left untreated) with 64 μM oxPt for 48 h before the increase in cell death (64 μM/0 μM) was determined by LDH. Results are displayed relative to control cells (set to 1; mean±s.e.m. from n =3 experiments; * P ≤0.05, t -test). ( f , g ) HCC2998, Colo205, DLD1, HT29 and LoVo CRC cells were treated for 1 h with MAPK11/14 inhibitors SB203580 (10 μM, blue) or SB202190 (5 μM, purple) then exposed to 64 μM oxPt (or left unexposed) for 48 h before the increase in cell death (64 μM/0 μM) was determined by LDH. Displayed relative to DMSO-treated cells (mean±s.e.m. from n =3–4 experiments with ‘*' indicating a significant reduction, P ≤0.05, t -test). ( h ) A schematic model showing how miR-625-3p mediated downregulation of MAP2K6 could modulate response to oxPt by abrogating MAPK14 stress-induced signalling. In the canonical model MAP2K6 in complex with MAP2K3 phosphorylates and activates MAPK14, which in turn—directly or indirectly via substrate kinases such as MAPKAPK2—activates a diverse number of target proteins central to stress-induced transcription, translation, cell cycle control and apoptosis.

    Article Snippet: Chemical inhibitors SB203580 (Invivogen) and SB202190 (Invivogen) were dissolved in dimethyl sulphoxide (DMSO) and kept in aliquots at −20 °C until use.

    Techniques: Inhibition, Transfection, Western Blot, Activity Assay, Expressing, Generated

    Danusertib induces autophagy via PI3K-mediated and p38 MAPK-mediated signaling pathways determined by flow cytometry. Notes: AGS and NCI-N78 cells were pretreated with SB202190 and WM for one hour and then incubated with danusertib for another 24 hours in the presence or absence of 0.5 μM danusertib. The cell samples were subjected to flow cytometry. ( A ) Flow cytometric plots showing autophagy of AGS and NCI-N78 cells and ( B ) bar graphs showing the percentage of autophagic AGS and NCI-N78 cells. Data represent the mean ± standard deviation of three independent experiments. ** P

    Journal: Drug Design, Development and Therapy

    Article Title: Danusertib, a potent pan-Aurora kinase and ABL kinase inhibitor, induces cell cycle arrest and programmed cell death and inhibits epithelial to mesenchymal transition involving the PI3K/Akt/mTOR-mediated signaling pathway in human gastric cancer AGS and NCI-N78 cells

    doi: 10.2147/DDDT.S74964

    Figure Lengend Snippet: Danusertib induces autophagy via PI3K-mediated and p38 MAPK-mediated signaling pathways determined by flow cytometry. Notes: AGS and NCI-N78 cells were pretreated with SB202190 and WM for one hour and then incubated with danusertib for another 24 hours in the presence or absence of 0.5 μM danusertib. The cell samples were subjected to flow cytometry. ( A ) Flow cytometric plots showing autophagy of AGS and NCI-N78 cells and ( B ) bar graphs showing the percentage of autophagic AGS and NCI-N78 cells. Data represent the mean ± standard deviation of three independent experiments. ** P

    Article Snippet: SB202190, 4-(4-fluorophenyl)-2- (4-hydroxyphe nyl)-5-(4-pyridyl)1H -imidazole, a selective inhibitor of p38 mitogen-activated protein kinase (MAPK), used as an autophagy inducer, and wortmannin (WM, a potent, irreversible, and selective phosphatidylinositol 3-kinase [phosphatidylinositol-4 5-bisphosphate 3-kinase] inhibitor and a blocker of autophagosome formation) were obtained from InvivoGen Inc (San Diego, CA, USA).

    Techniques: Flow Cytometry, Cytometry, Incubation, Standard Deviation

    Danusertib induces autophagy via PI3K-mediated and p38 MAPK-mediated signaling determined by confocal microscopy. Notes: AGS and NCI-N78 cells were pretreated with SB202190 and WM for one hour and then incubated for another 24 hours in the presence or absence of 0.5 μM danusertib. The cell samples were subjected to confocal microscopy. ( A ) Representative images showing autophagy of AGS and NCI-N78 cells and ( B ) bar graphs showing the percentage of autophagic AGS and NCI-N78 cells. Data represent the mean ± standard deviation of three independent experiments. Magnification 60×; scale bar 5 μM. * P

    Journal: Drug Design, Development and Therapy

    Article Title: Danusertib, a potent pan-Aurora kinase and ABL kinase inhibitor, induces cell cycle arrest and programmed cell death and inhibits epithelial to mesenchymal transition involving the PI3K/Akt/mTOR-mediated signaling pathway in human gastric cancer AGS and NCI-N78 cells

    doi: 10.2147/DDDT.S74964

    Figure Lengend Snippet: Danusertib induces autophagy via PI3K-mediated and p38 MAPK-mediated signaling determined by confocal microscopy. Notes: AGS and NCI-N78 cells were pretreated with SB202190 and WM for one hour and then incubated for another 24 hours in the presence or absence of 0.5 μM danusertib. The cell samples were subjected to confocal microscopy. ( A ) Representative images showing autophagy of AGS and NCI-N78 cells and ( B ) bar graphs showing the percentage of autophagic AGS and NCI-N78 cells. Data represent the mean ± standard deviation of three independent experiments. Magnification 60×; scale bar 5 μM. * P

    Article Snippet: SB202190, 4-(4-fluorophenyl)-2- (4-hydroxyphe nyl)-5-(4-pyridyl)1H -imidazole, a selective inhibitor of p38 mitogen-activated protein kinase (MAPK), used as an autophagy inducer, and wortmannin (WM, a potent, irreversible, and selective phosphatidylinositol 3-kinase [phosphatidylinositol-4 5-bisphosphate 3-kinase] inhibitor and a blocker of autophagosome formation) were obtained from InvivoGen Inc (San Diego, CA, USA).

    Techniques: Confocal Microscopy, Incubation, Standard Deviation

    ALS induces autophagy via PI3K-mediated and p38 MAPK-mediated signaling pathways in AGS and NCI-N78 cells. Notes: AGS and NCI-N78 cells were pretreated with SB202190 or wortmannin for 1 hour and then incubated for another 24 hours in the presence or absence of 1 μM ALS. ( A ) Representative images show autophagy of AGS and NCI-N78 cells. ( B ) Bar graphs show the percentage of autophagic AGS and NCI-N78 cells. Data are the mean ± SD of three independent experiments. * P

    Journal: Drug Design, Development and Therapy

    Article Title: Inhibition of mitotic Aurora kinase A by alisertib induces apoptosis and autophagy of human gastric cancer AGS and NCI-N78 cells

    doi: 10.2147/DDDT.S74127

    Figure Lengend Snippet: ALS induces autophagy via PI3K-mediated and p38 MAPK-mediated signaling pathways in AGS and NCI-N78 cells. Notes: AGS and NCI-N78 cells were pretreated with SB202190 or wortmannin for 1 hour and then incubated for another 24 hours in the presence or absence of 1 μM ALS. ( A ) Representative images show autophagy of AGS and NCI-N78 cells. ( B ) Bar graphs show the percentage of autophagic AGS and NCI-N78 cells. Data are the mean ± SD of three independent experiments. * P

    Article Snippet: SB202190 (4-[4-fluorophenyl]-2-[4-hydroxyphenyl]-5-[4-pyridyl]1H -imidazole, a selective inhibitor of p38 mitogen-activated protein kinase [MAPK] used as an autophagy inducer) and wortmannin (WM, a potent, irreversible, and selective PI3K inhibitor and a blocker of autophagosome formation) were purchased from Invivogen Inc (San Diego, CA, USA).

    Techniques: Incubation