Structured Review

LC Laboratories sb202190
Suppression ­­­of p38 signaling restores sensitivity to PIM inhibition in primary AML cells and mouse xenografts A.-B. Inhibition of p38 enhances AZD1208 response in primary AML cells. Patient cells were treated with increasing concentrations of AZD1208 (x-axis) and co-treated with 0.313 μM, 1.25 μM, or 5 μM SCIO-469. Growth was measured after 4 days using MTT. A day 0 measurement was used as a baseline value (y-axis = ‘0’) for growth. Negative relative growth indicates a cytotoxic effect ( n = 2). C. Combined p38/PIM inhibition suppresses mTOR signaling. Primary AML cells were treated for 24 hours with 1 μM AZD1208, 10 μM SCIO-469, or the combination. Cell lysates were harvested and subjected to western blot analysis. D.-G. Inhibition of p38 enhances AZD1208 response in a validation set of primary AML cells. Cells were treated with increasing concentrations of AZD1208 (x-axis) and co-treated with 0.3 μM, 1 μM, or 3 μM SCIO-469. Viability was measured after 72 hours using CellTiter-Glo. A day 0 measurement was used as a baseline value (y-axis = ‘0’) for growth. Negative relative growth indicates a cytotoxic effect ( n = 2). H. SCIO-469 is synergistic with AZD1208. Primary AML cells were treated with 2-fold dilutions of AZD1208, SCIO-469, or the combination. Viability was assessed by CellTiter-Blue and used to calculate synergy scores. I. Dual PIM/p38 inhibition suppresses tumor growth in a xenograft model. K562 cells (5.10 6 ) were subcutaneously implanted in Rag2 −/− IL2γc −/− mice. Once tumors were established, animals were treated with vehicle, AZD1208 (30 mg/kg), <t>SB202190</t> (5 mg/kg), or both drugs in combination. J. Mean tumor volume after 18 days treatment. Vehicle ( n = 11), AZD1208 ( n = 12), SB202190 ( n = 18), and combination ( n = 14). P -values were calculated via one-way ANOVA and Dunnett's test.
Sb202190, supplied by LC Laboratories, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Images

1) Product Images from "Intrinsic resistance to PIM kinase inhibition in AML through p38α-mediated feedback activation of mTOR signaling"

Article Title: Intrinsic resistance to PIM kinase inhibition in AML through p38α-mediated feedback activation of mTOR signaling

Journal: Oncotarget

doi: 10.18632/oncotarget.9822

Suppression ­­­of p38 signaling restores sensitivity to PIM inhibition in primary AML cells and mouse xenografts A.-B. Inhibition of p38 enhances AZD1208 response in primary AML cells. Patient cells were treated with increasing concentrations of AZD1208 (x-axis) and co-treated with 0.313 μM, 1.25 μM, or 5 μM SCIO-469. Growth was measured after 4 days using MTT. A day 0 measurement was used as a baseline value (y-axis = ‘0’) for growth. Negative relative growth indicates a cytotoxic effect ( n = 2). C. Combined p38/PIM inhibition suppresses mTOR signaling. Primary AML cells were treated for 24 hours with 1 μM AZD1208, 10 μM SCIO-469, or the combination. Cell lysates were harvested and subjected to western blot analysis. D.-G. Inhibition of p38 enhances AZD1208 response in a validation set of primary AML cells. Cells were treated with increasing concentrations of AZD1208 (x-axis) and co-treated with 0.3 μM, 1 μM, or 3 μM SCIO-469. Viability was measured after 72 hours using CellTiter-Glo. A day 0 measurement was used as a baseline value (y-axis = ‘0’) for growth. Negative relative growth indicates a cytotoxic effect ( n = 2). H. SCIO-469 is synergistic with AZD1208. Primary AML cells were treated with 2-fold dilutions of AZD1208, SCIO-469, or the combination. Viability was assessed by CellTiter-Blue and used to calculate synergy scores. I. Dual PIM/p38 inhibition suppresses tumor growth in a xenograft model. K562 cells (5.10 6 ) were subcutaneously implanted in Rag2 −/− IL2γc −/− mice. Once tumors were established, animals were treated with vehicle, AZD1208 (30 mg/kg), SB202190 (5 mg/kg), or both drugs in combination. J. Mean tumor volume after 18 days treatment. Vehicle ( n = 11), AZD1208 ( n = 12), SB202190 ( n = 18), and combination ( n = 14). P -values were calculated via one-way ANOVA and Dunnett's test.
Figure Legend Snippet: Suppression ­­­of p38 signaling restores sensitivity to PIM inhibition in primary AML cells and mouse xenografts A.-B. Inhibition of p38 enhances AZD1208 response in primary AML cells. Patient cells were treated with increasing concentrations of AZD1208 (x-axis) and co-treated with 0.313 μM, 1.25 μM, or 5 μM SCIO-469. Growth was measured after 4 days using MTT. A day 0 measurement was used as a baseline value (y-axis = ‘0’) for growth. Negative relative growth indicates a cytotoxic effect ( n = 2). C. Combined p38/PIM inhibition suppresses mTOR signaling. Primary AML cells were treated for 24 hours with 1 μM AZD1208, 10 μM SCIO-469, or the combination. Cell lysates were harvested and subjected to western blot analysis. D.-G. Inhibition of p38 enhances AZD1208 response in a validation set of primary AML cells. Cells were treated with increasing concentrations of AZD1208 (x-axis) and co-treated with 0.3 μM, 1 μM, or 3 μM SCIO-469. Viability was measured after 72 hours using CellTiter-Glo. A day 0 measurement was used as a baseline value (y-axis = ‘0’) for growth. Negative relative growth indicates a cytotoxic effect ( n = 2). H. SCIO-469 is synergistic with AZD1208. Primary AML cells were treated with 2-fold dilutions of AZD1208, SCIO-469, or the combination. Viability was assessed by CellTiter-Blue and used to calculate synergy scores. I. Dual PIM/p38 inhibition suppresses tumor growth in a xenograft model. K562 cells (5.10 6 ) were subcutaneously implanted in Rag2 −/− IL2γc −/− mice. Once tumors were established, animals were treated with vehicle, AZD1208 (30 mg/kg), SB202190 (5 mg/kg), or both drugs in combination. J. Mean tumor volume after 18 days treatment. Vehicle ( n = 11), AZD1208 ( n = 12), SB202190 ( n = 18), and combination ( n = 14). P -values were calculated via one-way ANOVA and Dunnett's test.

Techniques Used: Inhibition, MTT Assay, Western Blot, Mouse Assay

Pharmacological inhibition of p38 synergizes with AZD1208 through reduced mTOR signaling A.-E. p38 inhibitors enhance AZD1208 response. OCI-M1, OCI-M2, U2932, K562, and TMD8 cells were treated with increasing concentrations of AZD1208 (x-axis) and co-treated with the p38 inhibitor SB202190. Viability was measured after 5 days using CellTiter-Blue ( n = 3). F. p38 inhibitors are synergistic with AZD1208. OCI-M1, OCI-M2, U2932, K562, and TMD8 cells were treated with 2-fold dilutions of AZD1208, SB202190, SCIO-469, or combinations for 5 days. Viability was assessed by CellTiter-Blue and used to calculate synergy scores. Self-self combination treatments were used as a baseline to determine significance ( n = 3). P-values were calculated using a one-way ANOVA and Dunnett's test. p ≤ 0.05 (*), p ≤ 0.01 (**), p ≤ 0.001 (***), and p ≤ 0.0001 (****) G. Combined inhibition of PIM and p38 results in reduced AKT/mTOR signaling after 48 hours. OCI-M1 (2.10 5 cells/well in 6-well plate) and OCI-M2 (4.10 5 cells/well in 6-well plate) cells were treated for 48 hours with 2 μM AZD1208, 20 μM SB202190, or the combination. Cell lysates were harvested and subjected to western blot analysis ( n = 3).
Figure Legend Snippet: Pharmacological inhibition of p38 synergizes with AZD1208 through reduced mTOR signaling A.-E. p38 inhibitors enhance AZD1208 response. OCI-M1, OCI-M2, U2932, K562, and TMD8 cells were treated with increasing concentrations of AZD1208 (x-axis) and co-treated with the p38 inhibitor SB202190. Viability was measured after 5 days using CellTiter-Blue ( n = 3). F. p38 inhibitors are synergistic with AZD1208. OCI-M1, OCI-M2, U2932, K562, and TMD8 cells were treated with 2-fold dilutions of AZD1208, SB202190, SCIO-469, or combinations for 5 days. Viability was assessed by CellTiter-Blue and used to calculate synergy scores. Self-self combination treatments were used as a baseline to determine significance ( n = 3). P-values were calculated using a one-way ANOVA and Dunnett's test. p ≤ 0.05 (*), p ≤ 0.01 (**), p ≤ 0.001 (***), and p ≤ 0.0001 (****) G. Combined inhibition of PIM and p38 results in reduced AKT/mTOR signaling after 48 hours. OCI-M1 (2.10 5 cells/well in 6-well plate) and OCI-M2 (4.10 5 cells/well in 6-well plate) cells were treated for 48 hours with 2 μM AZD1208, 20 μM SB202190, or the combination. Cell lysates were harvested and subjected to western blot analysis ( n = 3).

Techniques Used: Inhibition, Western Blot

2) Product Images from "Caspase-3 suppresses diethylnitrosamine-induced hepatocyte death, compensatory proliferation and hepatocarcinogenesis through inhibiting p38 activation"

Article Title: Caspase-3 suppresses diethylnitrosamine-induced hepatocyte death, compensatory proliferation and hepatocarcinogenesis through inhibiting p38 activation

Journal: Cell Death & Disease

doi: 10.1038/s41419-018-0617-7

Inhibition of p38 abrogated enhanced DEN-induced hepatocyte death, compensatory proliferation and HCC development induced by deletion of Caspase-3 . a Expression of p-p38 and GAPDH proteins in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by western blotting. b Apoptosis in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by TUNEL staining. Bars: 20 µM. c Quantification of TUNEL staining for ( b ) ( n = 3). d Quantification of Ki67 staining in the livers of Caspase-3 KO mice 3 days after injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190. e Photographs of livers of WT and Caspase-3 KO mice 9 months after DEN injection with or without SB202190. f Quantification of liver tumor numbers ( n = 5) and liver tumor sizes ( n = 5) for ( e ). Values in ( c ), ( d ) and ( f ) are means ± SDs
Figure Legend Snippet: Inhibition of p38 abrogated enhanced DEN-induced hepatocyte death, compensatory proliferation and HCC development induced by deletion of Caspase-3 . a Expression of p-p38 and GAPDH proteins in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by western blotting. b Apoptosis in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by TUNEL staining. Bars: 20 µM. c Quantification of TUNEL staining for ( b ) ( n = 3). d Quantification of Ki67 staining in the livers of Caspase-3 KO mice 3 days after injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190. e Photographs of livers of WT and Caspase-3 KO mice 9 months after DEN injection with or without SB202190. f Quantification of liver tumor numbers ( n = 5) and liver tumor sizes ( n = 5) for ( e ). Values in ( c ), ( d ) and ( f ) are means ± SDs

Techniques Used: Inhibition, Expressing, Mouse Assay, Injection, Western Blot, TUNEL Assay, Staining

3) Product Images from "Opposing roles of p38 and JNK in a Drosophila model of TDP-43 proteinopathy reveal oxidative stress and innate immunity as pathogenic components of neurodegeneration"

Article Title: Opposing roles of p38 and JNK in a Drosophila model of TDP-43 proteinopathy reveal oxidative stress and innate immunity as pathogenic components of neurodegeneration

Journal: Human Molecular Genetics

doi: 10.1093/hmg/ddu493

Pharmacological and genetic inhibition of p38 suppress TDP-43 toxicity during adulthood. ( A ) Survival curve of adult male D42 > TDP-43 flies treated with the p38 inhibitor SB202190 at 10, 100 and 200 μ m (concentration in food). Median survival
Figure Legend Snippet: Pharmacological and genetic inhibition of p38 suppress TDP-43 toxicity during adulthood. ( A ) Survival curve of adult male D42 > TDP-43 flies treated with the p38 inhibitor SB202190 at 10, 100 and 200 μ m (concentration in food). Median survival

Techniques Used: Inhibition, Concentration Assay

4) Product Images from "Caspase-3 suppresses diethylnitrosamine-induced hepatocyte death, compensatory proliferation and hepatocarcinogenesis through inhibiting p38 activation"

Article Title: Caspase-3 suppresses diethylnitrosamine-induced hepatocyte death, compensatory proliferation and hepatocarcinogenesis through inhibiting p38 activation

Journal: Cell Death & Disease

doi: 10.1038/s41419-018-0617-7

Inhibition of p38 abrogated enhanced DEN-induced hepatocyte death, compensatory proliferation and HCC development induced by deletion of Caspase-3 . a Expression of p-p38 and GAPDH proteins in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by western blotting. b Apoptosis in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by TUNEL staining. Bars: 20 µM. c Quantification of TUNEL staining for ( b ) ( n = 3). d Quantification of Ki67 staining in the livers of Caspase-3 KO mice 3 days after injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190. e Photographs of livers of WT and Caspase-3 KO mice 9 months after DEN injection with or without SB202190. f Quantification of liver tumor numbers ( n = 5) and liver tumor sizes ( n = 5) for ( e ). Values in ( c ), ( d ) and ( f ) are means ± SDs
Figure Legend Snippet: Inhibition of p38 abrogated enhanced DEN-induced hepatocyte death, compensatory proliferation and HCC development induced by deletion of Caspase-3 . a Expression of p-p38 and GAPDH proteins in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by western blotting. b Apoptosis in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by TUNEL staining. Bars: 20 µM. c Quantification of TUNEL staining for ( b ) ( n = 3). d Quantification of Ki67 staining in the livers of Caspase-3 KO mice 3 days after injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190. e Photographs of livers of WT and Caspase-3 KO mice 9 months after DEN injection with or without SB202190. f Quantification of liver tumor numbers ( n = 5) and liver tumor sizes ( n = 5) for ( e ). Values in ( c ), ( d ) and ( f ) are means ± SDs

Techniques Used: Inhibition, Expressing, Mouse Assay, Injection, Western Blot, TUNEL Assay, Staining

5) Product Images from "Caspase-3 suppresses diethylnitrosamine-induced hepatocyte death, compensatory proliferation and hepatocarcinogenesis through inhibiting p38 activation"

Article Title: Caspase-3 suppresses diethylnitrosamine-induced hepatocyte death, compensatory proliferation and hepatocarcinogenesis through inhibiting p38 activation

Journal: Cell Death & Disease

doi: 10.1038/s41419-018-0617-7

Inhibition of p38 abrogated enhanced DEN-induced hepatocyte death, compensatory proliferation and HCC development induced by deletion of Caspase-3 . a Expression of p-p38 and GAPDH proteins in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by western blotting. b Apoptosis in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by TUNEL staining. Bars: 20 µM. c Quantification of TUNEL staining for ( b ) ( n = 3). d Quantification of Ki67 staining in the livers of Caspase-3 KO mice 3 days after injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190. e Photographs of livers of WT and Caspase-3 KO mice 9 months after DEN injection with or without SB202190. f Quantification of liver tumor numbers ( n = 5) and liver tumor sizes ( n = 5) for ( e ). Values in ( c ), ( d ) and ( f ) are means ± SDs
Figure Legend Snippet: Inhibition of p38 abrogated enhanced DEN-induced hepatocyte death, compensatory proliferation and HCC development induced by deletion of Caspase-3 . a Expression of p-p38 and GAPDH proteins in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by western blotting. b Apoptosis in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by TUNEL staining. Bars: 20 µM. c Quantification of TUNEL staining for ( b ) ( n = 3). d Quantification of Ki67 staining in the livers of Caspase-3 KO mice 3 days after injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190. e Photographs of livers of WT and Caspase-3 KO mice 9 months after DEN injection with or without SB202190. f Quantification of liver tumor numbers ( n = 5) and liver tumor sizes ( n = 5) for ( e ). Values in ( c ), ( d ) and ( f ) are means ± SDs

Techniques Used: Inhibition, Expressing, Mouse Assay, Injection, Western Blot, TUNEL Assay, Staining

6) Product Images from "Caspase-3 suppresses diethylnitrosamine-induced hepatocyte death, compensatory proliferation and hepatocarcinogenesis through inhibiting p38 activation"

Article Title: Caspase-3 suppresses diethylnitrosamine-induced hepatocyte death, compensatory proliferation and hepatocarcinogenesis through inhibiting p38 activation

Journal: Cell Death & Disease

doi: 10.1038/s41419-018-0617-7

Inhibition of p38 abrogated enhanced DEN-induced hepatocyte death, compensatory proliferation and HCC development induced by deletion of Caspase-3 . a Expression of p-p38 and GAPDH proteins in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by western blotting. b Apoptosis in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by TUNEL staining. Bars: 20 µM. c Quantification of TUNEL staining for ( b ) ( n = 3). d Quantification of Ki67 staining in the livers of Caspase-3 KO mice 3 days after injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190. e Photographs of livers of WT and Caspase-3 KO mice 9 months after DEN injection with or without SB202190. f Quantification of liver tumor numbers ( n = 5) and liver tumor sizes ( n = 5) for ( e ). Values in ( c ), ( d ) and ( f ) are means ± SDs
Figure Legend Snippet: Inhibition of p38 abrogated enhanced DEN-induced hepatocyte death, compensatory proliferation and HCC development induced by deletion of Caspase-3 . a Expression of p-p38 and GAPDH proteins in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by western blotting. b Apoptosis in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by TUNEL staining. Bars: 20 µM. c Quantification of TUNEL staining for ( b ) ( n = 3). d Quantification of Ki67 staining in the livers of Caspase-3 KO mice 3 days after injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190. e Photographs of livers of WT and Caspase-3 KO mice 9 months after DEN injection with or without SB202190. f Quantification of liver tumor numbers ( n = 5) and liver tumor sizes ( n = 5) for ( e ). Values in ( c ), ( d ) and ( f ) are means ± SDs

Techniques Used: Inhibition, Expressing, Mouse Assay, Injection, Western Blot, TUNEL Assay, Staining

7) Product Images from "Cryptotanshinone Activates p38/JNK and Inhibits Erk1/2 Leading to Caspase-Independent Cell Death in Tumor Cells"

Article Title: Cryptotanshinone Activates p38/JNK and Inhibits Erk1/2 Leading to Caspase-Independent Cell Death in Tumor Cells

Journal: Cancer prevention research (Philadelphia, Pa.)

doi: 10.1158/1940-6207.CAPR-11-0551

CPT-induced cell death is in part by activation of p38/JNK and inhibition Erk1/2. A–C, DU145 cells, grown in 6-well plates (A and B) or 96-well plates (C), were pretreated with or without SB202190 (10 μmol/L) or SP600125 (20 μmol/L)
Figure Legend Snippet: CPT-induced cell death is in part by activation of p38/JNK and inhibition Erk1/2. A–C, DU145 cells, grown in 6-well plates (A and B) or 96-well plates (C), were pretreated with or without SB202190 (10 μmol/L) or SP600125 (20 μmol/L)

Techniques Used: Cycling Probe Technology, Activation Assay, Inhibition

Related Articles

Mouse Assay:

Article Title: Caspase-3 suppresses diethylnitrosamine-induced hepatocyte death, compensatory proliferation and hepatocarcinogenesis through inhibiting p38 activation
Article Snippet: For p38 inhibitor treatments, SB202190 (LC Laboratories, Cat # S-1700) was diluted in 6% captisol (CyDex, Inc., Lenexa, KS). .. One day prior to DEN treatment, six 2-week-old or 8- to 12-week-old WT and six 2-week-old or 8- to 12-week-old Casp3 −/− mice were administered vehicle solution (6% captisol) or 20 mg/kg SB202190 by i.p. daily for 3 days and livers were collected 9 months, 3 or 10 days after DEN treatment. .. Isolation and culture of primary mouse hepatocytes Hepatocytes from Casp3 +/+ and Casp3 −/− mice were isolated by the non-recirculating two-step perfusion method as previously described .

Article Title: Intrinsic resistance to PIM kinase inhibition in AML through p38α-mediated feedback activation of mTOR signaling
Article Snippet: K562 cells (5.106 ) were subcutaneously implanted with matrigel (BD Bioscience) into the right flank of mice. .. When tumor size reached ~50 to 100 mm3 , mice were randomly assigned and treated once daily with 30 mg/kg AZD1208 (AstraZeneca) by oral gavage and/or 5 mg/kg SB202190 (LC Laboratories) by intraperitoneal injection. ..

Injection:

Article Title: Intrinsic resistance to PIM kinase inhibition in AML through p38α-mediated feedback activation of mTOR signaling
Article Snippet: K562 cells (5.106 ) were subcutaneously implanted with matrigel (BD Bioscience) into the right flank of mice. .. When tumor size reached ~50 to 100 mm3 , mice were randomly assigned and treated once daily with 30 mg/kg AZD1208 (AstraZeneca) by oral gavage and/or 5 mg/kg SB202190 (LC Laboratories) by intraperitoneal injection. ..

Multiple Displacement Amplification:

Article Title: A Signaling Network Controlling Androgenic Repression of c-Fos Protein in Prostate Adenocarcinoma Cells *
Article Snippet: Here we utilized TPA to investigate androgen control of c-Fos expression in prostate cancer cells to elucidate the molecular mechanism of androgenic control of c-Fos expression and to develop new insights into the therapeutic control of CRPC. .. The sources were as follows: anti-phospho-MEK1 (Ser-217/221, #9121), anti-ERK1/2 (#9107) anti-phospho-ERK1/2 (Thr-202/204, #9101S), anti-phospho(P)-ELK-1 (Ser-383, #9181), anti-P-PKCμ (Ser-744/748, #2054), anti-P-PKCμ (Ser-916, #2051), anti-P-PKCδ (Thr-643, #9376), anti-P-PKCδ (Thr-505, #9374), P-SRF (Ser-103, #4261), and anti-Mcl-1 (#5453) (Cell Signaling Technology); mouse anti-ELK-1 (#sc-65986), rabbit anti-ELK (sc-335) and anti-SRF (sc-335), anti-MEK1 (sc-219), anti-c-Fos (sc-7202), anti-tubulin (sc-5286), and anti-AR (sc-7035 and sc-816) (Santa Cruz Biotechnology); anti-PKCμ (# ) anti-PKCδ (# ), anti-PKCα (# ), anti-PKCϵ (# ), anti-PCKζ (# ), anti-PKCι (# ), anti-PKCγ (# ), and anti-PKCτ (#P1512) (BD Transduction Laboratories); p38MAPK (Upstate Biotechnology); anti-phospho-p38MAPK (Thr-180/Tyr-182) (Zymed Laboratories Inc.); anti-β-actin (#A-5441), DHT (#D-5027), and TPA (#P8139) (Sigma-Aldrich); pGL3-basic-luciferase (Promega); characterized FBS and dextran-charcoal-stripped FBS (HyClone); R1881 (#NLP005005, PerkinElmer Life Sciences); U0216, PD98059, SP600125, SB202190, SB203580, GF109203X, selumetinib, and ZSTK474 (LC Laboratories); MK2206 (ChemieTek); pFC-MEK1 (Stratagene); LNCaP, VCaP, DU145, RWPE-1, and MDA-PCa-2b (ATCC); C4-2 and C4-2B (Leland Chung); and CWR22Rv1 (James Jacobberger and Mike Sramkoski). ..

Concentration Assay:

Article Title: Regulation of Transforming Growth Factor-?1-Dependent Integrin ?6 Expression by p38 Mitogen-Activated Protein Kinase in Bile Duct Epithelial Cells
Article Snippet: Before treatment, MMNK-1 cells were grown to 70% confluence and serum-starved for 1 h before stimulation with 5 ng/ml TGF-β1 or its vehicle [0.1% BSA (Thermo Fisher Scientific) in endotoxin-free PBS (Sigma-Aldrich)]. .. For inhibitor studies, MMNK-1 cells were serum-starved for 30 min, and then pretreated with 10 μM SB203580, SB202190, or SB202474 (LC Laboratories), 10 μg/ml cycloheximide (Sigma-Aldrich), or DMSO vehicle (final concentration, 0.1%) for an additional 30 min before treatment with 5 ng/ml TGF-β1 or vehicle. .. For dominant-negative mutant studies, cells were grown to 50% confluence, transfected with 1 μg of plasmid using Fugene6 transfection reagent, allowed to incubate for 24 h to reach 70% confluence, and treated as described above.

other:

Article Title: Ubiquitin plays an atypical role in GPCR-induced p38 MAP kinase activation on endosomes
Article Snippet: SB203580 and SB202190 (p38 inhibitors) and U0126 (MEK inhibitor) were from LC laboratories.

Article Title: Opposing roles of p38 and JNK in a Drosophila model of TDP-43 proteinopathy reveal oxidative stress and innate immunity as pathogenic components of neurodegeneration
Article Snippet: For SB202190 (LC laboratories) and SB203580 (LC laboratories) treatment experiments, adult male D42 > TDP-43 flies were maintained in medium containing 10, 100 or 200 μ m of each inhibitor.

Expressing:

Article Title: Regulation of Transforming Growth Factor-?1-Dependent Integrin ?6 Expression by p38 Mitogen-Activated Protein Kinase in Bile Duct Epithelial Cells
Article Snippet: Pretreatment of MMNK-1 cells with SB203580 significantly reduced Itgβ6 mRNA expression in MMNK-1 cells treated with TGF-β1 by 40% ( C). .. Likewise, pretreatment with a more potent p38 MAPK inhibitor, SB202190, significantly reduced Itgβ6 mRNA expression in MMNK-1 cells treated with TGF-β1 by 70% ( D). .. In contrast, pretreatment with a structurally related negative control compound for these two inhibitors (SB202474) had no effect ( E).

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    LC Laboratories sb202190
    Inhibition of p38 abrogated enhanced DEN-induced hepatocyte death, compensatory proliferation and HCC development induced by deletion of Caspase-3 . a Expression of p-p38 and GAPDH proteins in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg <t>SB202190</t> was analyzed by western blotting. b Apoptosis in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by TUNEL staining. Bars: 20 µM. c Quantification of TUNEL staining for ( b ) ( n = 3). d Quantification of Ki67 staining in the livers of Caspase-3 KO mice 3 days after injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190. e Photographs of livers of WT and Caspase-3 KO mice 9 months after DEN injection with or without SB202190. f Quantification of liver tumor numbers ( n = 5) and liver tumor sizes ( n = 5) for ( e ). Values in ( c ), ( d ) and ( f ) are means ± SDs
    Sb202190, supplied by LC Laboratories, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Inhibition of p38 abrogated enhanced DEN-induced hepatocyte death, compensatory proliferation and HCC development induced by deletion of Caspase-3 . a Expression of p-p38 and GAPDH proteins in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by western blotting. b Apoptosis in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by TUNEL staining. Bars: 20 µM. c Quantification of TUNEL staining for ( b ) ( n = 3). d Quantification of Ki67 staining in the livers of Caspase-3 KO mice 3 days after injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190. e Photographs of livers of WT and Caspase-3 KO mice 9 months after DEN injection with or without SB202190. f Quantification of liver tumor numbers ( n = 5) and liver tumor sizes ( n = 5) for ( e ). Values in ( c ), ( d ) and ( f ) are means ± SDs

    Journal: Cell Death & Disease

    Article Title: Caspase-3 suppresses diethylnitrosamine-induced hepatocyte death, compensatory proliferation and hepatocarcinogenesis through inhibiting p38 activation

    doi: 10.1038/s41419-018-0617-7

    Figure Lengend Snippet: Inhibition of p38 abrogated enhanced DEN-induced hepatocyte death, compensatory proliferation and HCC development induced by deletion of Caspase-3 . a Expression of p-p38 and GAPDH proteins in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by western blotting. b Apoptosis in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by TUNEL staining. Bars: 20 µM. c Quantification of TUNEL staining for ( b ) ( n = 3). d Quantification of Ki67 staining in the livers of Caspase-3 KO mice 3 days after injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190. e Photographs of livers of WT and Caspase-3 KO mice 9 months after DEN injection with or without SB202190. f Quantification of liver tumor numbers ( n = 5) and liver tumor sizes ( n = 5) for ( e ). Values in ( c ), ( d ) and ( f ) are means ± SDs

    Article Snippet: For p38 inhibitor treatments, SB202190 (LC Laboratories, Cat # S-1700) was diluted in 6% captisol (CyDex, Inc., Lenexa, KS).

    Techniques: Inhibition, Expressing, Mouse Assay, Injection, Western Blot, TUNEL Assay, Staining

    Inhibition of p38 abrogated enhanced DEN-induced hepatocyte death, compensatory proliferation and HCC development induced by deletion of Caspase-3 . a Expression of p-p38 and GAPDH proteins in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by western blotting. b Apoptosis in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by TUNEL staining. Bars: 20 µM. c Quantification of TUNEL staining for ( b ) ( n = 3). d Quantification of Ki67 staining in the livers of Caspase-3 KO mice 3 days after injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190. e Photographs of livers of WT and Caspase-3 KO mice 9 months after DEN injection with or without SB202190. f Quantification of liver tumor numbers ( n = 5) and liver tumor sizes ( n = 5) for ( e ). Values in ( c ), ( d ) and ( f ) are means ± SDs

    Journal: Cell Death & Disease

    Article Title: Caspase-3 suppresses diethylnitrosamine-induced hepatocyte death, compensatory proliferation and hepatocarcinogenesis through inhibiting p38 activation

    doi: 10.1038/s41419-018-0617-7

    Figure Lengend Snippet: Inhibition of p38 abrogated enhanced DEN-induced hepatocyte death, compensatory proliferation and HCC development induced by deletion of Caspase-3 . a Expression of p-p38 and GAPDH proteins in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by western blotting. b Apoptosis in the livers of Caspase-3 KO mice 3 days following injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190 was analyzed by TUNEL staining. Bars: 20 µM. c Quantification of TUNEL staining for ( b ) ( n = 3). d Quantification of Ki67 staining in the livers of Caspase-3 KO mice 3 days after injection with either saline (Un) or 100 mg/kg DEN plus 20 mg/kg SB202190. e Photographs of livers of WT and Caspase-3 KO mice 9 months after DEN injection with or without SB202190. f Quantification of liver tumor numbers ( n = 5) and liver tumor sizes ( n = 5) for ( e ). Values in ( c ), ( d ) and ( f ) are means ± SDs

    Article Snippet: For p38 inhibitor treatments, SB202190 (LC Laboratories, Cat # S-1700) was diluted in 6% captisol (CyDex, Inc., Lenexa, KS).

    Techniques: Inhibition, Expressing, Mouse Assay, Injection, Western Blot, TUNEL Assay, Staining

    Suppression ­­­of p38 signaling restores sensitivity to PIM inhibition in primary AML cells and mouse xenografts A.-B. Inhibition of p38 enhances AZD1208 response in primary AML cells. Patient cells were treated with increasing concentrations of AZD1208 (x-axis) and co-treated with 0.313 μM, 1.25 μM, or 5 μM SCIO-469. Growth was measured after 4 days using MTT. A day 0 measurement was used as a baseline value (y-axis = ‘0’) for growth. Negative relative growth indicates a cytotoxic effect ( n = 2). C. Combined p38/PIM inhibition suppresses mTOR signaling. Primary AML cells were treated for 24 hours with 1 μM AZD1208, 10 μM SCIO-469, or the combination. Cell lysates were harvested and subjected to western blot analysis. D.-G. Inhibition of p38 enhances AZD1208 response in a validation set of primary AML cells. Cells were treated with increasing concentrations of AZD1208 (x-axis) and co-treated with 0.3 μM, 1 μM, or 3 μM SCIO-469. Viability was measured after 72 hours using CellTiter-Glo. A day 0 measurement was used as a baseline value (y-axis = ‘0’) for growth. Negative relative growth indicates a cytotoxic effect ( n = 2). H. SCIO-469 is synergistic with AZD1208. Primary AML cells were treated with 2-fold dilutions of AZD1208, SCIO-469, or the combination. Viability was assessed by CellTiter-Blue and used to calculate synergy scores. I. Dual PIM/p38 inhibition suppresses tumor growth in a xenograft model. K562 cells (5.10 6 ) were subcutaneously implanted in Rag2 −/− IL2γc −/− mice. Once tumors were established, animals were treated with vehicle, AZD1208 (30 mg/kg), SB202190 (5 mg/kg), or both drugs in combination. J. Mean tumor volume after 18 days treatment. Vehicle ( n = 11), AZD1208 ( n = 12), SB202190 ( n = 18), and combination ( n = 14). P -values were calculated via one-way ANOVA and Dunnett's test.

    Journal: Oncotarget

    Article Title: Intrinsic resistance to PIM kinase inhibition in AML through p38α-mediated feedback activation of mTOR signaling

    doi: 10.18632/oncotarget.9822

    Figure Lengend Snippet: Suppression ­­­of p38 signaling restores sensitivity to PIM inhibition in primary AML cells and mouse xenografts A.-B. Inhibition of p38 enhances AZD1208 response in primary AML cells. Patient cells were treated with increasing concentrations of AZD1208 (x-axis) and co-treated with 0.313 μM, 1.25 μM, or 5 μM SCIO-469. Growth was measured after 4 days using MTT. A day 0 measurement was used as a baseline value (y-axis = ‘0’) for growth. Negative relative growth indicates a cytotoxic effect ( n = 2). C. Combined p38/PIM inhibition suppresses mTOR signaling. Primary AML cells were treated for 24 hours with 1 μM AZD1208, 10 μM SCIO-469, or the combination. Cell lysates were harvested and subjected to western blot analysis. D.-G. Inhibition of p38 enhances AZD1208 response in a validation set of primary AML cells. Cells were treated with increasing concentrations of AZD1208 (x-axis) and co-treated with 0.3 μM, 1 μM, or 3 μM SCIO-469. Viability was measured after 72 hours using CellTiter-Glo. A day 0 measurement was used as a baseline value (y-axis = ‘0’) for growth. Negative relative growth indicates a cytotoxic effect ( n = 2). H. SCIO-469 is synergistic with AZD1208. Primary AML cells were treated with 2-fold dilutions of AZD1208, SCIO-469, or the combination. Viability was assessed by CellTiter-Blue and used to calculate synergy scores. I. Dual PIM/p38 inhibition suppresses tumor growth in a xenograft model. K562 cells (5.10 6 ) were subcutaneously implanted in Rag2 −/− IL2γc −/− mice. Once tumors were established, animals were treated with vehicle, AZD1208 (30 mg/kg), SB202190 (5 mg/kg), or both drugs in combination. J. Mean tumor volume after 18 days treatment. Vehicle ( n = 11), AZD1208 ( n = 12), SB202190 ( n = 18), and combination ( n = 14). P -values were calculated via one-way ANOVA and Dunnett's test.

    Article Snippet: When tumor size reached ~50 to 100 mm3 , mice were randomly assigned and treated once daily with 30 mg/kg AZD1208 (AstraZeneca) by oral gavage and/or 5 mg/kg SB202190 (LC Laboratories) by intraperitoneal injection.

    Techniques: Inhibition, MTT Assay, Western Blot, Mouse Assay

    Pharmacological inhibition of p38 synergizes with AZD1208 through reduced mTOR signaling A.-E. p38 inhibitors enhance AZD1208 response. OCI-M1, OCI-M2, U2932, K562, and TMD8 cells were treated with increasing concentrations of AZD1208 (x-axis) and co-treated with the p38 inhibitor SB202190. Viability was measured after 5 days using CellTiter-Blue ( n = 3). F. p38 inhibitors are synergistic with AZD1208. OCI-M1, OCI-M2, U2932, K562, and TMD8 cells were treated with 2-fold dilutions of AZD1208, SB202190, SCIO-469, or combinations for 5 days. Viability was assessed by CellTiter-Blue and used to calculate synergy scores. Self-self combination treatments were used as a baseline to determine significance ( n = 3). P-values were calculated using a one-way ANOVA and Dunnett's test. p ≤ 0.05 (*), p ≤ 0.01 (**), p ≤ 0.001 (***), and p ≤ 0.0001 (****) G. Combined inhibition of PIM and p38 results in reduced AKT/mTOR signaling after 48 hours. OCI-M1 (2.10 5 cells/well in 6-well plate) and OCI-M2 (4.10 5 cells/well in 6-well plate) cells were treated for 48 hours with 2 μM AZD1208, 20 μM SB202190, or the combination. Cell lysates were harvested and subjected to western blot analysis ( n = 3).

    Journal: Oncotarget

    Article Title: Intrinsic resistance to PIM kinase inhibition in AML through p38α-mediated feedback activation of mTOR signaling

    doi: 10.18632/oncotarget.9822

    Figure Lengend Snippet: Pharmacological inhibition of p38 synergizes with AZD1208 through reduced mTOR signaling A.-E. p38 inhibitors enhance AZD1208 response. OCI-M1, OCI-M2, U2932, K562, and TMD8 cells were treated with increasing concentrations of AZD1208 (x-axis) and co-treated with the p38 inhibitor SB202190. Viability was measured after 5 days using CellTiter-Blue ( n = 3). F. p38 inhibitors are synergistic with AZD1208. OCI-M1, OCI-M2, U2932, K562, and TMD8 cells were treated with 2-fold dilutions of AZD1208, SB202190, SCIO-469, or combinations for 5 days. Viability was assessed by CellTiter-Blue and used to calculate synergy scores. Self-self combination treatments were used as a baseline to determine significance ( n = 3). P-values were calculated using a one-way ANOVA and Dunnett's test. p ≤ 0.05 (*), p ≤ 0.01 (**), p ≤ 0.001 (***), and p ≤ 0.0001 (****) G. Combined inhibition of PIM and p38 results in reduced AKT/mTOR signaling after 48 hours. OCI-M1 (2.10 5 cells/well in 6-well plate) and OCI-M2 (4.10 5 cells/well in 6-well plate) cells were treated for 48 hours with 2 μM AZD1208, 20 μM SB202190, or the combination. Cell lysates were harvested and subjected to western blot analysis ( n = 3).

    Article Snippet: When tumor size reached ~50 to 100 mm3 , mice were randomly assigned and treated once daily with 30 mg/kg AZD1208 (AstraZeneca) by oral gavage and/or 5 mg/kg SB202190 (LC Laboratories) by intraperitoneal injection.

    Techniques: Inhibition, Western Blot