sb202190 (Millipore)

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SB 202190

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S7067

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SB 202190 was used to inhibit p38 activation in MCF7 cells5, mouse macrophages6 and HepG2 cells.7

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Millipore sb202190
SB 202190

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sb202190 - by Bioz Stars, 2021-05

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Images

1) Product Images from "SB203580 increases G-CSF production via a stem-loop destabilizing element in the 3’ untranslated region in macrophages independently of its effect on p38 MAPK activity"

Article Title: SB203580 increases G-CSF production via a stem-loop destabilizing element in the 3’ untranslated region in macrophages independently of its effect on p38 MAPK activity

Journal: Journal of Biomedical Science

doi: 10.1186/s12929-016-0221-z

Effects of various p38 MAPK inhibitors on LPS-induced G-CSF mRNA in RAW264.7 and THP-1 macrophages. RAW264.7 cells ( a ) and THP-1 ( b ) were pretreated for 30 min with DMSO or 10 μM SB203580, SB202190, PD169316, SB239063, or SKF86002, then 100 ng/ml of LPS was added and incubation continued for 6 h, then the G-CSF mRNA levels were determined by RT-qPCR, normalized to GAPDH mRNA levels, and expressed relative to the value in the DMSO control, set as 1. The values are the mean ± SD for three separate experiments. * p

Figure Legend Snippet: Effects of various p38 MAPK inhibitors on LPS-induced G-CSF mRNA in RAW264.7 and THP-1 macrophages. RAW264.7 cells ( a ) and THP-1 ( b ) were pretreated for 30 min with DMSO or 10 μM SB203580, SB202190, PD169316, SB239063, or SKF86002, then 100 ng/ml of LPS was added and incubation continued for 6 h, then the G-CSF mRNA levels were determined by RT-qPCR, normalized to GAPDH mRNA levels, and expressed relative to the value in the DMSO control, set as 1. The values are the mean ± SD for three separate experiments. * p

Techniques Used: Incubation, Quantitative RT-PCR

2) Product Images from "The anti-tumor efficacy of 2-deoxyglucose and D-allose are enhanced with p38 inhibition in pancreatic and ovarian cell lines"

Article Title: The anti-tumor efficacy of 2-deoxyglucose and D-allose are enhanced with p38 inhibition in pancreatic and ovarian cell lines

Journal: Journal of Experimental & Clinical Cancer Research : CR

doi: 10.1186/s13046-015-0147-4

SB202190 enhances cleavage of PARP when combined with glucose analogs. Western blot analysis of whole cell lysates from cells treated for 24 hours with 2-DG or D-allose alone or in combination with SB202190. Lysates were probed for cleaved and total PARP. Tubulin served as a loading control for protein. Cleaved PARP band density was quantified using ImageJ software with normalization to α-Tubulin. One representative experiment is shown, n = 3.

Figure Legend Snippet: SB202190 enhances cleavage of PARP when combined with glucose analogs. Western blot analysis of whole cell lysates from cells treated for 24 hours with 2-DG or D-allose alone or in combination with SB202190. Lysates were probed for cleaved and total PARP. Tubulin served as a loading control for protein. Cleaved PARP band density was quantified using ImageJ software with normalization to α-Tubulin. One representative experiment is shown, n = 3.

Techniques Used: Western Blot, Software

Effect of dosing regimens on the proliferation of pancreatic and ovarian cell lines following 48 hours of treatment. Cells were treated with increasing doses of 2-DG or D-allose alone or in combination with oxaliplatin (pancreatic cell lines), cisplatin (ovarian cell lines) and/or SB202190. Cell proliferation was measured using the MTT assay. The ratio of 2-DG or D-allose to the platinum analogs was 2000:1 for all doses, respectively. One representative experiment is shown, n = 6.

Figure Legend Snippet: Effect of dosing regimens on the proliferation of pancreatic and ovarian cell lines following 48 hours of treatment. Cells were treated with increasing doses of 2-DG or D-allose alone or in combination with oxaliplatin (pancreatic cell lines), cisplatin (ovarian cell lines) and/or SB202190. Cell proliferation was measured using the MTT assay. The ratio of 2-DG or D-allose to the platinum analogs was 2000:1 for all doses, respectively. One representative experiment is shown, n = 6.

Techniques Used: MTT Assay

Lactate production and HIF-1α expression in pancreatic cancer cell lines. A) . Effect of 2-DG and D-allose alone or in combination with SB202190 following 24 hours of treatment on lactate production measured in cell culture media or in cells. Values are normalized to total cell protein. One representative experiment is shown, n = 3. *p

Figure Legend Snippet: Lactate production and HIF-1α expression in pancreatic cancer cell lines. A) . Effect of 2-DG and D-allose alone or in combination with SB202190 following 24 hours of treatment on lactate production measured in cell culture media or in cells. Values are normalized to total cell protein. One representative experiment is shown, n = 3. *p

Techniques Used: Expressing, Cell Culture

HIF-1α transcriptional activity is modulated by SB202190. A) . MIA PaCa-2 cells were stably transfected with a HRE-luciferase reporter and treated for 3 24, and 48 hours with 2-DG or D-allose alone and in combination with SB202190. Luciferase activity was normalized to total protein. One representative experiment is shown, n = 3. *Indicates a p

Figure Legend Snippet: HIF-1α transcriptional activity is modulated by SB202190. A) . MIA PaCa-2 cells were stably transfected with a HRE-luciferase reporter and treated for 3 24, and 48 hours with 2-DG or D-allose alone and in combination with SB202190. Luciferase activity was normalized to total protein. One representative experiment is shown, n = 3. *Indicates a p

Techniques Used: Activity Assay, Stable Transfection, Transfection, Luciferase

3) Product Images from "Vascular Endothelial Growth Factor Receptor-2 Couples Cyclo-Oxygenase-2 with Pro-Angiogenic Actions of Leptin on Human Endothelial Cells"

Article Title: Vascular Endothelial Growth Factor Receptor-2 Couples Cyclo-Oxygenase-2 with Pro-Angiogenic Actions of Leptin on Human Endothelial Cells

Journal: PLoS ONE

doi: 10.1371/journal.pone.0018823

Leptin-stimulated endothelial cell migration is attenuated by blockade of p38 MAPK , Akt or COX-2 activities. A. Confluent monolayers of quiescent HUVEC were scratch wounded and treated with either vehicle (control), leptin (1–100 ng/mL) or VEGF (25 ng/mL). The rate of wound closure was monitored in real time by confocal microscopy (B). C. Confluent cells were exposed to vehicle, leptin or VEGF in the presence or absence of NS398, SB202190 or LY294002 (1 µmol/L), wounded, and migration monitored (18 h). Data in B and C are mean ± SEM of 3 separate experiments with duplicate observations per treatment. * p

Figure Legend Snippet: Leptin-stimulated endothelial cell migration is attenuated by blockade of p38 MAPK , Akt or COX-2 activities. A. Confluent monolayers of quiescent HUVEC were scratch wounded and treated with either vehicle (control), leptin (1–100 ng/mL) or VEGF (25 ng/mL). The rate of wound closure was monitored in real time by confocal microscopy (B). C. Confluent cells were exposed to vehicle, leptin or VEGF in the presence or absence of NS398, SB202190 or LY294002 (1 µmol/L), wounded, and migration monitored (18 h). Data in B and C are mean ± SEM of 3 separate experiments with duplicate observations per treatment. * p

Techniques Used: Migration, Confocal Microscopy

Leptin-induced capillary-like tube formation on matrigel requires activation of p38 MAPK and Akt, and is COX-dependent. HUVEC were cultured on growth-factor reduced matrigel and treated with either vehicle, leptin (1–100 ng/mL) or VEGF (25 ng/mL) in the presence or absence of 1 µmol/L NS398, SB202190 or LY294002 for 8 hours. Cells were photographed (magnification: ×5) and the number of tubes counted. Each treatment was carried out in duplicate in 3 separate experiments. A. Representative images; B. Analysis of tube number expressed as fold increase (± SEM) compared to control. *** p

Figure Legend Snippet: Leptin-induced capillary-like tube formation on matrigel requires activation of p38 MAPK and Akt, and is COX-dependent. HUVEC were cultured on growth-factor reduced matrigel and treated with either vehicle, leptin (1–100 ng/mL) or VEGF (25 ng/mL) in the presence or absence of 1 µmol/L NS398, SB202190 or LY294002 for 8 hours. Cells were photographed (magnification: ×5) and the number of tubes counted. Each treatment was carried out in duplicate in 3 separate experiments. A. Representative images; B. Analysis of tube number expressed as fold increase (± SEM) compared to control. *** p

Techniques Used: Activation Assay, Cell Culture

4) Product Images from "Stress-Induced Enzyme Activation Primes Murine Embryonic Stem Cells to Differentiate Toward the First Extraembryonic Lineage"

Article Title: Stress-Induced Enzyme Activation Primes Murine Embryonic Stem Cells to Differentiate Toward the First Extraembryonic Lineage

Journal: Stem Cells and Development

doi: 10.1089/scd.2014.0157

JNK-dependent signaling suppressed Rex1 expression during 24 h of hyperosmotic stress. (A) mESCs were incubated±200 mM sorbitol for 0–24 h± (A) p38MAPK inhibitor SB202190 (10 μM) or PI3K inhibitor

Figure Legend Snippet: JNK-dependent signaling suppressed Rex1 expression during 24 h of hyperosmotic stress. (A) mESCs were incubated±200 mM sorbitol for 0–24 h± (A) p38MAPK inhibitor SB202190 (10 μM) or PI3K inhibitor

Techniques Used: Expressing, Incubation

Efficacy of enzyme inhibitors during hyperosmotic stress. mESCs were incubated for 4 h in the presence of 200 mM sorbitol with or without one of the enzyme inhibitors SB202190 (p38), PD98059 (MEK1), U0126 (MEK1/2), L-JNKi-1 (JNK), AKTi

Figure Legend Snippet: Efficacy of enzyme inhibitors during hyperosmotic stress. mESCs were incubated for 4 h in the presence of 200 mM sorbitol with or without one of the enzyme inhibitors SB202190 (p38), PD98059 (MEK1), U0126 (MEK1/2), L-JNKi-1 (JNK), AKTi

Techniques Used: Incubation

p38MAPK rescues pluripotency of mESCs during 24 h of hyperosmotic stress. (A) mESCs were incubated ±200 mM sorbitol for 0–24 h and ±p38 inhibitor SB202190 (10 μM). mESCs were lysed, and proteins

Figure Legend Snippet: p38MAPK rescues pluripotency of mESCs during 24 h of hyperosmotic stress. (A) mESCs were incubated ±200 mM sorbitol for 0–24 h and ±p38 inhibitor SB202190 (10 μM). mESCs were lysed, and proteins

Techniques Used: Incubation

5) Product Images from "Response and Resistance to MEK Inhibition in Leukaemias Initiated by Hyperactive Ras"

Article Title: Response and Resistance to MEK Inhibition in Leukaemias Initiated by Hyperactive Ras

Journal: Nature

doi: 10.1038/nature08279

Genetic and functional analysis of AML #6537 associate reduced p38α kinase activity with resistance to MEK inhibition a , Southern blot analysis of MOL4070LTR integrations of AML #6537 following treatment with vehicle (V), CI-1040 (CI) or PD0325901 (PD). Asterisks denote restriction fragments that are present in all the resistant AMLs, but are not seen in the sensitive leukaemia. b , Southern blot analysis of paired sensitive and resistant AML #6537 with a Mapk14 probe. The resistant leukaemias shown in lanes CI and PD show a Mapk14 hybridization fragment, which overlaps with one of the MOL4070LTR bands in the resistant leukaemias shown in panel a . c , Basal p38 kinase activity of resistant AML #6537 cells (solid line) is reduced in comparison to the parental leukaemia (heavy dashed line), but remains elevated above WT bone marrow cells (dotted line). This is a representative example of 3 independent experiments. d , SB202190 (SB), a p38α inhibitor, antagonizes the ability of CI-1040 (CI) to reduce blast colony inhibition in parental AML #6537 (solid white bars, n=7) in the presence of GM-CSF (GM). Blast colony growth of sensitive AML #6537 is significantly increased by the addition of SB to CI-1040 (*p= 0.0043; unpaired t-test). By contrast, CI-1040 (2.5 µM) has a inhibitory effect on WT CFU-GM colony (solid black bars, n=8) and resistant AML #6537 (chequered bars, n=5) blast colony growth, which is not affected by 2.5 µM SB202190. Error bars represent the s.e.m.

Figure Legend Snippet: Genetic and functional analysis of AML #6537 associate reduced p38α kinase activity with resistance to MEK inhibition a , Southern blot analysis of MOL4070LTR integrations of AML #6537 following treatment with vehicle (V), CI-1040 (CI) or PD0325901 (PD). Asterisks denote restriction fragments that are present in all the resistant AMLs, but are not seen in the sensitive leukaemia. b , Southern blot analysis of paired sensitive and resistant AML #6537 with a Mapk14 probe. The resistant leukaemias shown in lanes CI and PD show a Mapk14 hybridization fragment, which overlaps with one of the MOL4070LTR bands in the resistant leukaemias shown in panel a . c , Basal p38 kinase activity of resistant AML #6537 cells (solid line) is reduced in comparison to the parental leukaemia (heavy dashed line), but remains elevated above WT bone marrow cells (dotted line). This is a representative example of 3 independent experiments. d , SB202190 (SB), a p38α inhibitor, antagonizes the ability of CI-1040 (CI) to reduce blast colony inhibition in parental AML #6537 (solid white bars, n=7) in the presence of GM-CSF (GM). Blast colony growth of sensitive AML #6537 is significantly increased by the addition of SB to CI-1040 (*p= 0.0043; unpaired t-test). By contrast, CI-1040 (2.5 µM) has a inhibitory effect on WT CFU-GM colony (solid black bars, n=8) and resistant AML #6537 (chequered bars, n=5) blast colony growth, which is not affected by 2.5 µM SB202190. Error bars represent the s.e.m.

Techniques Used: Functional Assay, Activity Assay, Inhibition, Southern Blot, Hybridization

6) Product Images from "Shape-Induced Terminal Differentiation of Human Epidermal Stem Cells Requires p38 and Is Regulated by Histone Acetylation"

Article Title: Shape-Induced Terminal Differentiation of Human Epidermal Stem Cells Requires p38 and Is Regulated by Histone Acetylation

Journal: PLoS ONE

doi: 10.1371/journal.pone.0027259

Effect of p38 inhibition on SRF signaling. (A) SRF transcriptional activity in human keratinocytes expressing the SRF luciferase reporter and TK renilla control. Cells were treated overnight with 2 µM SB202190 or carrier, then 1 µM cytochalasin D or carrier for 7 h. Data are means ± SEM of 4 replicates from one experiment (representative of 3 independent experiments). *P

Figure Legend Snippet: Effect of p38 inhibition on SRF signaling. (A) SRF transcriptional activity in human keratinocytes expressing the SRF luciferase reporter and TK renilla control. Cells were treated overnight with 2 µM SB202190 or carrier, then 1 µM cytochalasin D or carrier for 7 h. Data are means ± SEM of 4 replicates from one experiment (representative of 3 independent experiments). *P

Techniques Used: Inhibition, Activity Assay, Expressing, Luciferase

Effect of p38 inhibition on cytoskeletal organization and MRTF-A localization. (A) Representative images of paxillin (green) and F-actin (red) localization in keratinocytes treated with carrier or 2 µM SB202190 for 24 h. Scale bar = 20 µm (B) Representative image of MRTF-A localization in keratinocytes transfected with FLAG-MRTF-A construct, treated overnight with or without SB202190 and then stimulated with 1 µM cytochalasin D for 1 h. MRTF-A was detected by immunofluorescence staining for the FLAG tag. N = 20 cells examined per condition. Scale bar = 50 µm.

Figure Legend Snippet: Effect of p38 inhibition on cytoskeletal organization and MRTF-A localization. (A) Representative images of paxillin (green) and F-actin (red) localization in keratinocytes treated with carrier or 2 µM SB202190 for 24 h. Scale bar = 20 µm (B) Representative image of MRTF-A localization in keratinocytes transfected with FLAG-MRTF-A construct, treated overnight with or without SB202190 and then stimulated with 1 µM cytochalasin D for 1 h. MRTF-A was detected by immunofluorescence staining for the FLAG tag. N = 20 cells examined per condition. Scale bar = 50 µm.

Techniques Used: Inhibition, Transfection, Construct, Immunofluorescence, Staining, FLAG-tag

Effect of p38 inhibition on epidermal stem cell gene expression. Real-time RT-PCR detection of (A) LRIG1 , (B) TP63 , (C) DLL1 , and (D) ITGB1 mRNA levels for cells on micro-patterned substrates. Cells were seeded onto 20 µm islands and allowed to adhere for 1 h before rinsing and treating with carrier or 2 µM SB202190. Expression levels were normalized to the 1 h time point and represent the means ± SEM of 3 experiments.

Figure Legend Snippet: Effect of p38 inhibition on epidermal stem cell gene expression. Real-time RT-PCR detection of (A) LRIG1 , (B) TP63 , (C) DLL1 , and (D) ITGB1 mRNA levels for cells on micro-patterned substrates. Cells were seeded onto 20 µm islands and allowed to adhere for 1 h before rinsing and treating with carrier or 2 µM SB202190. Expression levels were normalized to the 1 h time point and represent the means ± SEM of 3 experiments.

Techniques Used: Inhibition, Expressing, Quantitative RT-PCR

Effect of MAPK inhibitors on shape-induced terminal differentiation. (A) Representative images of keratinocytes on micro-patterned substrates comprising 20 µm diameter collagen islands. Cells were cultured for 24 h in medium containing carrier (0.1% DMSO), 10 µM PD169316, 2 µM SB202190, 10 µM SP600125, or 10 µM PD98059. Immunofluorescence staining for involucrin (green) shows terminally differentiating cells, and nuclei are labeled with DAPI (blue). Scale bar = 50 µm. Quantification of (B-C) involucrin, (D) transglutaminase I, and (E) Ki67 positive cells after 24 h on 20 µm or 50 µm substrates. In (C), the proportion of involucrin positive cells was normalized to carrier-treated cells on 20 µm islands. Data are means ± SEM of 3 experiments. *P

Figure Legend Snippet: Effect of MAPK inhibitors on shape-induced terminal differentiation. (A) Representative images of keratinocytes on micro-patterned substrates comprising 20 µm diameter collagen islands. Cells were cultured for 24 h in medium containing carrier (0.1% DMSO), 10 µM PD169316, 2 µM SB202190, 10 µM SP600125, or 10 µM PD98059. Immunofluorescence staining for involucrin (green) shows terminally differentiating cells, and nuclei are labeled with DAPI (blue). Scale bar = 50 µm. Quantification of (B-C) involucrin, (D) transglutaminase I, and (E) Ki67 positive cells after 24 h on 20 µm or 50 µm substrates. In (C), the proportion of involucrin positive cells was normalized to carrier-treated cells on 20 µm islands. Data are means ± SEM of 3 experiments. *P

Techniques Used: Cell Culture, Immunofluorescence, Staining, Labeling

Role of histone acetylation in SRF signaling. (A) SRF transcriptional activity in human keratinocytes expressing the SRF luciferase reporter and TK renilla control. Cells were treated overnight with or without 2 µM SB202190 or 200 nM TSA, then stimulated for 7 h with 10% FBS. Data are means ± SEM of 4 replicates from one experiment (representative of 3 independent experiments). *P

Figure Legend Snippet: Role of histone acetylation in SRF signaling. (A) SRF transcriptional activity in human keratinocytes expressing the SRF luciferase reporter and TK renilla control. Cells were treated overnight with or without 2 µM SB202190 or 200 nM TSA, then stimulated for 7 h with 10% FBS. Data are means ± SEM of 4 replicates from one experiment (representative of 3 independent experiments). *P

Techniques Used: Activity Assay, Expressing, Luciferase

7) Product Images from "EGF regulates plasminogen activator inhibitor-1 (PAI-1) by a pathway involving c-Src, PKC?, and sphingosine kinase 1 in glioblastoma cells"

Article Title: EGF regulates plasminogen activator inhibitor-1 (PAI-1) by a pathway involving c-Src, PKC?, and sphingosine kinase 1 in glioblastoma cells

Journal:

doi: 10.1096/fj.07-8276com

Inhibition of PKC prevents up-regulation of PAI-1 expression by EGF. A172 cells were pretreated with 10 µM LY294002, 1 µM U0126, 10 µM SB202190, 1 µM SP600125, 100 nM staurosporin, 5 µM BAY11–7082 ( A ), the

Figure Legend Snippet: Inhibition of PKC prevents up-regulation of PAI-1 expression by EGF. A172 cells were pretreated with 10 µM LY294002, 1 µM U0126, 10 µM SB202190, 1 µM SP600125, 100 nM staurosporin, 5 µM BAY11–7082 ( A ), the

Techniques Used: Inhibition, Expressing

8) Product Images from "The anti-tumor efficacy of 2-deoxyglucose and D-allose are enhanced with p38 inhibition in pancreatic and ovarian cell lines"

Article Title: The anti-tumor efficacy of 2-deoxyglucose and D-allose are enhanced with p38 inhibition in pancreatic and ovarian cell lines

Journal: Journal of Experimental & Clinical Cancer Research : CR

doi: 10.1186/s13046-015-0147-4

Techniques Used: Western Blot, Software

Techniques Used: MTT Assay

Techniques Used: Expressing, Cell Culture

Techniques Used: Activity Assay, Stable Transfection, Transfection, Luciferase

9) Product Images from "Clostridium difficile Toxins A and B Directly Stimulate Human Mast Cells ▿"

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

Journal: Infection and Immunity

doi: 10.1128/IAI.00195-07

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

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

Techniques Used:

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

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

Techniques Used: Activation Assay, Inhibition

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

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

Techniques Used: Standard Deviation, Inhibition

10) Product Images from "Computational and In Vitro Analysis of Plumbagin’s Molecular Mechanism for the Treatment of Hepatocellular Carcinoma"

Article Title: Computational and In Vitro Analysis of Plumbagin’s Molecular Mechanism for the Treatment of Hepatocellular Carcinoma

Journal: Frontiers in Pharmacology

doi: 10.3389/fphar.2021.594833

(A) Protein expression levels of LC3-I, LC3-II, p38 MAPK, and p-p38 MAPK in SMMC-7721 cells measured by Western blot after treatment with 5 μM PL, 10 μM 3-MA autophagy inhibitor, 10 μM rapamycin autophagy agonist, 10 μM SB202190, and 10 μM SB203580 p38 MAPK inhibitor. (B) LC3-I, LC3-II, p38 MAPK, and p-p38 MAPK were used as internal reference total proteins for gray value analysis. * p

Figure Legend Snippet: (A) Protein expression levels of LC3-I, LC3-II, p38 MAPK, and p-p38 MAPK in SMMC-7721 cells measured by Western blot after treatment with 5 μM PL, 10 μM 3-MA autophagy inhibitor, 10 μM rapamycin autophagy agonist, 10 μM SB202190, and 10 μM SB203580 p38 MAPK inhibitor. (B) LC3-I, LC3-II, p38 MAPK, and p-p38 MAPK were used as internal reference total proteins for gray value analysis. * p

Techniques Used: Expressing, Western Blot

11) Product Images from "Tuning of Protein Kinase Circuitry by p38α Is Vital for Epithelial Tissue Homeostasis *"

Article Title: Tuning of Protein Kinase Circuitry by p38α Is Vital for Epithelial Tissue Homeostasis *

Journal: The Journal of Biological Chemistry

doi: 10.1074/jbc.M113.452029

Inhibition of p38α kinase activity results in TAK1 hyperactivation via affecting TAK1 ubiquitination and turnover. A , RAW264.7 mouse macrophage cells were preincubated with dimethyl sulfoxide ( DMSO ; 0.1%), SC409 (10 μ m ), and SB202190 (10

Figure Legend Snippet: Inhibition of p38α kinase activity results in TAK1 hyperactivation via affecting TAK1 ubiquitination and turnover. A , RAW264.7 mouse macrophage cells were preincubated with dimethyl sulfoxide ( DMSO ; 0.1%), SC409 (10 μ m ), and SB202190 (10

Techniques Used: Inhibition, Activity Assay

12) Product Images from "Natural Compound Mixture, Containing Emodin, Genipin, Chlorogenic Acid, Cimigenoside, and Ginsenoside Rb1, Ameliorates Psoriasis-Like Skin Lesions by Suppressing Inflammation and Proliferation in Keratinocytes"

Article Title: Natural Compound Mixture, Containing Emodin, Genipin, Chlorogenic Acid, Cimigenoside, and Ginsenoside Rb1, Ameliorates Psoriasis-Like Skin Lesions by Suppressing Inflammation and Proliferation in Keratinocytes

Journal: Evidence-based Complementary and Alternative Medicine : eCAM

doi: 10.1155/2020/9416962

Effects of PSM on the proinflammatory chemokine expression and related signaling pathways in M5-stimulated HaCaT cells. (a) HaCaT cells were pretreated with emodin, genipin, chlorogenic, cimigenoside, ginsenoside Rb1 (10 μ M), PSM (50 μ M), or dexamethasone (DEX, 10 μ M) for 1 h and then stimulated with M5 (IL-1 α , IL-17A, IL-22, oncostatin M, and TNF- α , 10 ng/ml each) for 24 h. The CXCL8, CXCL10, and CCL20 levels in the culture supernatants were determined using commercial ELISA kits. (b) The effects of PSM on cell viability was assessed using an XTT assay. HaCaT cells were treated with emodin, genipin, chlorogenic, cimigenoside, ginsenoside Rb1, or PSM (10, 50 μ M) for 24 h. (c) HaCaT cells were pretreated with PSM (50 μ M) or DEX (10 μ M) for 1 h and then stimulated with M5 for 30 min. Protein expression of p-ERK, p-p38, p-JNK, and p-STAT3 were assessed by Western blotting, and the band intensities were normalized versus ERK, p38, JNK, and STAT3, respectively. (d) HaCaT cells were pretreated with U0126, SB202190, SP600125, and cryptotanshinone (10 μ M) for 1 h and then stimulated with M5 for 24 h. The CXCL8, CXCL10, and CCL20 levels in the culture supernatants were determined using commercial ELISA kits. # P

Figure Legend Snippet: Effects of PSM on the proinflammatory chemokine expression and related signaling pathways in M5-stimulated HaCaT cells. (a) HaCaT cells were pretreated with emodin, genipin, chlorogenic, cimigenoside, ginsenoside Rb1 (10 μ M), PSM (50 μ M), or dexamethasone (DEX, 10 μ M) for 1 h and then stimulated with M5 (IL-1 α , IL-17A, IL-22, oncostatin M, and TNF- α , 10 ng/ml each) for 24 h. The CXCL8, CXCL10, and CCL20 levels in the culture supernatants were determined using commercial ELISA kits. (b) The effects of PSM on cell viability was assessed using an XTT assay. HaCaT cells were treated with emodin, genipin, chlorogenic, cimigenoside, ginsenoside Rb1, or PSM (10, 50 μ M) for 24 h. (c) HaCaT cells were pretreated with PSM (50 μ M) or DEX (10 μ M) for 1 h and then stimulated with M5 for 30 min. Protein expression of p-ERK, p-p38, p-JNK, and p-STAT3 were assessed by Western blotting, and the band intensities were normalized versus ERK, p38, JNK, and STAT3, respectively. (d) HaCaT cells were pretreated with U0126, SB202190, SP600125, and cryptotanshinone (10 μ M) for 1 h and then stimulated with M5 for 24 h. The CXCL8, CXCL10, and CCL20 levels in the culture supernatants were determined using commercial ELISA kits. # P

Techniques Used: Expressing, Enzyme-linked Immunosorbent Assay, XTT Assay, Western Blot

13) Product Images from "Mitochondria-Derived Reactive Oxygen Species Mediate Heme Oxygenase-1 Expression in Sheared Endothelial Cells"

Article Title: Mitochondria-Derived Reactive Oxygen Species Mediate Heme Oxygenase-1 Expression in Sheared Endothelial Cells

Journal: The Journal of Pharmacology and Experimental Therapeutics

doi: 10.1124/jpet.108.145557

Effect of protein phosphorylation cascade inhibitors on shear-induced HO-1 expression. ECs were preincubated and sheared in the presence of wortmannin (500 nM), PD98059 (25 μM), or SB202190 (20 μM). Representative immunoblot for HO-1

Figure Legend Snippet: Effect of protein phosphorylation cascade inhibitors on shear-induced HO-1 expression. ECs were preincubated and sheared in the presence of wortmannin (500 nM), PD98059 (25 μM), or SB202190 (20 μM). Representative immunoblot for HO-1

Techniques Used: Expressing

14) Product Images from "The Artemisinin Derivative Artesunate Inhibits Corneal Neovascularization by Inducing ROS-Dependent Apoptosis in Vascular Endothelial Cells"

Article Title: The Artemisinin Derivative Artesunate Inhibits Corneal Neovascularization by Inducing ROS-Dependent Apoptosis in Vascular Endothelial Cells

Journal: Investigative Ophthalmology & Visual Science

doi: 10.1167/iovs.12-11068

ARS induced p38MAPK activation in HUVECs. ARS activated p38MAPK in time-dependent manner ( A ) and concentration-dependent manner ( B ). Specific p38MAPK inhibitors SB202190 and SB203580 inhibited ARS-activated p38MAPK ( C ). SB202190 and SB203580 protected cells from ARS-induced apoptosis ( D ) and ( E ). n = 3. ** denotes P

Figure Legend Snippet: ARS induced p38MAPK activation in HUVECs. ARS activated p38MAPK in time-dependent manner ( A ) and concentration-dependent manner ( B ). Specific p38MAPK inhibitors SB202190 and SB203580 inhibited ARS-activated p38MAPK ( C ). SB202190 and SB203580 protected cells from ARS-induced apoptosis ( D ) and ( E ). n = 3. ** denotes P

Techniques Used: Activation Assay, Concentration Assay

15) Product Images from "JNK and p38 Mitogen-Activated Protein Kinase Pathways Contribute to Porcine Circovirus Type 2 Infection ▿"

Article Title: JNK and p38 Mitogen-Activated Protein Kinase Pathways Contribute to Porcine Circovirus Type 2 Infection ▿

Journal: Journal of Virology

doi: 10.1128/JVI.00135-09

Inhibition of JNK1/2 and p38 MAPK phosphorylation reduces PCV2-induced caspase-3 activity. Whole-cell lysates harvested from PCV2-infected cells at 72 h after treatment with various concentrations of the JNK inhibitor 1 (A) or SB202190 (B), as well as

Figure Legend Snippet: Inhibition of JNK1/2 and p38 MAPK phosphorylation reduces PCV2-induced caspase-3 activity. Whole-cell lysates harvested from PCV2-infected cells at 72 h after treatment with various concentrations of the JNK inhibitor 1 (A) or SB202190 (B), as well as

Techniques Used: Inhibition, Activity Assay, Infection

Inhibition of JNK1/2 and p38 MAPK phosphorylation blocks PCV2 replication. Supernatants of PCV2-infected PK15 cells at 72 h after treatment with various concentrations of JNK inhibitor 1 (A) or SB202190 (B), as well as UV-irradiated PCV2-infected cell

Figure Legend Snippet: Inhibition of JNK1/2 and p38 MAPK phosphorylation blocks PCV2 replication. Supernatants of PCV2-infected PK15 cells at 72 h after treatment with various concentrations of JNK inhibitor 1 (A) or SB202190 (B), as well as UV-irradiated PCV2-infected cell

Techniques Used: Inhibition, Infection, Irradiation

16) Product Images from "Developmental Role of Macrophage Cannabinoid-1 Receptor Signaling in Type 2 Diabetes"

Article Title: Developmental Role of Macrophage Cannabinoid-1 Receptor Signaling in Type 2 Diabetes

Journal: Diabetes

doi: 10.2337/db16-1199

CB 1 R regulation of Irf5 expression and its role in β-cell loss in vivo. A : Irf5 mRNA levels in islets isolated from lean control (Ctrl) and ZDF rats treated for 4 weeks with vehicle (Veh) or 3 mg/kg/day JD5037. B : Irf5 mRNA levels in PECs isolated from wild-type or Cnr1 −/− mice exposed to vehicle or 5 μmol/L ACEA for 24 h. C : Irf5 mRNA in rat PECs treated with vehicle or 5 μmol/L ACEA alone or in the presence of 100 nmol/L JD5037, 100 ng/mL PTX, 25 μg/mL SB202190, or 25 μg/mL SP600125. D : ACEA-induced increase in IRF5 expression is not affected by MAPK14 knockdown. E : Effects of Irf5 knockdown on Cnr1 mRNA and on chemokine and cytokine secretion induced by 5 μmol/L ACEA in aliquots of 10 6 rat peritoneal macrophages. Points/columns and bars are the mean ± SEM from six rats/group. Significant differences from values in Veh (*) or Veh + ACEA groups (#). * P

Figure Legend Snippet: CB 1 R regulation of Irf5 expression and its role in β-cell loss in vivo. A : Irf5 mRNA levels in islets isolated from lean control (Ctrl) and ZDF rats treated for 4 weeks with vehicle (Veh) or 3 mg/kg/day JD5037. B : Irf5 mRNA levels in PECs isolated from wild-type or Cnr1 −/− mice exposed to vehicle or 5 μmol/L ACEA for 24 h. C : Irf5 mRNA in rat PECs treated with vehicle or 5 μmol/L ACEA alone or in the presence of 100 nmol/L JD5037, 100 ng/mL PTX, 25 μg/mL SB202190, or 25 μg/mL SP600125. D : ACEA-induced increase in IRF5 expression is not affected by MAPK14 knockdown. E : Effects of Irf5 knockdown on Cnr1 mRNA and on chemokine and cytokine secretion induced by 5 μmol/L ACEA in aliquots of 10 6 rat peritoneal macrophages. Points/columns and bars are the mean ± SEM from six rats/group. Significant differences from values in Veh (*) or Veh + ACEA groups (#). * P

Techniques Used: Expressing, In Vivo, Isolation, Mouse Assay

17) Product Images from "Regulation of cAMP Responsive Element Binding Protein 3-Like 1 (Creb3l1) Expression by Orphan Nuclear Receptor Nr4a1"

Article Title: Regulation of cAMP Responsive Element Binding Protein 3-Like 1 (Creb3l1) Expression by Orphan Nuclear Receptor Nr4a1

Journal: Frontiers in Molecular Neuroscience

doi: 10.3389/fnmol.2017.00413

Identification of Nr4a1 as a novel regulator of the Creb3l1 gene. (A) Immunofluorescent localization of Creb3l1 with Nr4a1 and c-Fos in magnocellular neurones of euhydrated and 3 days dehydrated rat. (B) The effect of c-Fos and Nr4a1 knockdown on basal expression of Creb3l1 were examined by qRT-PCR compared to a control NT shRNA cell line. (C) Responses of knockdown cell lines to 4 h time course of FSK treatment compared to a control NT shRNA cell line. (D) Immunoblot analysis of Creb3l1 expression in Nr4a1 knockdown cell lines treated with FSK. (E) The effect of pretreatment (2 h) of p38 inhibitor SB202190 on FSK-induced upregulation of Nr4a1 and Creb3l1 mRNA in AtT20 cells. NT, non-targeting; FSK, forskolin. Values are means + SEM of n = 3 per group. * p

Figure Legend Snippet: Identification of Nr4a1 as a novel regulator of the Creb3l1 gene. (A) Immunofluorescent localization of Creb3l1 with Nr4a1 and c-Fos in magnocellular neurones of euhydrated and 3 days dehydrated rat. (B) The effect of c-Fos and Nr4a1 knockdown on basal expression of Creb3l1 were examined by qRT-PCR compared to a control NT shRNA cell line. (C) Responses of knockdown cell lines to 4 h time course of FSK treatment compared to a control NT shRNA cell line. (D) Immunoblot analysis of Creb3l1 expression in Nr4a1 knockdown cell lines treated with FSK. (E) The effect of pretreatment (2 h) of p38 inhibitor SB202190 on FSK-induced upregulation of Nr4a1 and Creb3l1 mRNA in AtT20 cells. NT, non-targeting; FSK, forskolin. Values are means + SEM of n = 3 per group. * p

Techniques Used: Expressing, Quantitative RT-PCR, shRNA

Inhibition:

Article Title: Lipopolysaccharide-Induced Activation of ?2-Integrin Function in Macrophages Requires Irak Kinase Activity, p38 Mitogen- Activated Protein Kinase, and the Rap1 GTPase
Article Snippet: Pretreatment with SB202190 (0.1 to 10 μM) inhibited macrophage spreading induced by LPS in a dose-dependent way (Fig. A and B). .. A 50% inhibition of spreading was observed at concentrations between 0.1 and 0.5 μM, which is in agreement with the published 50% inhibitory concentration (IC50 ) of ∼0.3 μM for SB202190. .. To confirm the involvement of p38 in LPS-induced spreading, a cDNA construct encoding dominant-negative p38 was microinjected into macrophages prior to LPS treatment.

Article Title: Preferential Signaling and Induction of Allergy-promoting Lymphokines Upon Weak Stimulation of the High Affinity IgE Receptor on Mast Cells
Article Snippet: MCP-1 and TNF-α Genes Show Preferential Requirement for p38MAPK or ERK2, Respectively. .. While it is well understood that multiple pathways cooperate with the activity of MAP kinases in gene expression ( , ), we tested whether the mRNA accumulation of some cytokines and chemokines showed preferential sensitivity to inhibition of p38MAPK and ERK2 by SB202190 and PD98059, respectively. ..

Concentration Assay:

Article Title: The Plant-Derived Glucocorticoid Receptor Agonist Endiandrin A Acts as Co-Stimulator of Colonic Epithelial Sodium Channels (ENaC) via SGK-1 and MAPKs
Article Snippet: TNF-α (TEBU, Offenbach, Germany) was used in a concentration of 500 IU/ml or 10,000 IU/ml in PBS. .. Specific inhibitors of MAPK, the p38 MAPK inhibitor SB202190, the p42/44 extracellular signal-regulated kinase (ERK, ERK’s upstream kinase MEK1/2) inhibitor U0126 and the JNK MAPK inhibitor SP600125 (Sigma-Aldrich) were used in a concentration of 10 µM. .. For GR antagonization RU-486 (10 µM; Sigma-Aldrich) was used.

other:

Article Title: MEKK1 plays a critical role in activating the transcription factor C/EBP-?-dependent gene expression in response to IFN-?
Article Snippet: Murine IFN-γ (Roche Molecular Biochemicals); SB202190 (Calbiochem), U0126 (Promega), epidermal growth factor (EGF), eicosatetranoic acid, antibodies specific for phospho-ERK1/2; actin (Sigma); ERK2; ISGF3γ, MEKK1; and C/EBP-β (Santa Cruz Biotechnology) were used.