p38 inhibitor amg548 Search Results


92
Tocris amg 548
(A) Confluent Calu-3 cells underwent cyclic mechanical stretch for 24 h. Partial oxygen pressures (pO2) from supernatants were determined using I-STAT analyzer and compared to un-stretched controls (mean ± s.d., n = 3). (B) Following 8 or 24 h of cyclic mechanical stretch exposure, mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. Activity is given as OD (optical density) change over time (mean ± s.d., n = 3). (C) siRNA knockdown of succinate-CoA ligase (SUCLG). RT PCR for SUCLG from A549 cells after siRNA treatment compared with control siRNA treatment (CsiR; beta-actin was used as house-keeping gene; n = 3). Note: siRNA knockdown revealed 82% reduction of SUCLG transcript. (D) A549 cells following siRNA repression of succinate-CoA ligase (siSUCLG) or treatment with nonspecific control siRNA (CsiR) were stretched for 0 or 8 h, lysed, and blotted for HIF1A. One representative blot of three is displayed. (E) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without α-ketoglutarate (aKG) treatment. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed. (F–H) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 h with or without inhibitors of JNK, ERK, or <t>p38.</t> Mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. (I) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without neutralizing antibodies for TNFA or IL-6. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed.
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Amgen amg548
(A) Confluent Calu-3 cells underwent cyclic mechanical stretch for 24 h. Partial oxygen pressures (pO2) from supernatants were determined using I-STAT analyzer and compared to un-stretched controls (mean ± s.d., n = 3). (B) Following 8 or 24 h of cyclic mechanical stretch exposure, mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. Activity is given as OD (optical density) change over time (mean ± s.d., n = 3). (C) siRNA knockdown of succinate-CoA ligase (SUCLG). RT PCR for SUCLG from A549 cells after siRNA treatment compared with control siRNA treatment (CsiR; beta-actin was used as house-keeping gene; n = 3). Note: siRNA knockdown revealed 82% reduction of SUCLG transcript. (D) A549 cells following siRNA repression of succinate-CoA ligase (siSUCLG) or treatment with nonspecific control siRNA (CsiR) were stretched for 0 or 8 h, lysed, and blotted for HIF1A. One representative blot of three is displayed. (E) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without α-ketoglutarate (aKG) treatment. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed. (F–H) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 h with or without inhibitors of JNK, ERK, or <t>p38.</t> Mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. (I) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without neutralizing antibodies for TNFA or IL-6. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed.
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90
Scios Inc scio 323
(A) Confluent Calu-3 cells underwent cyclic mechanical stretch for 24 h. Partial oxygen pressures (pO2) from supernatants were determined using I-STAT analyzer and compared to un-stretched controls (mean ± s.d., n = 3). (B) Following 8 or 24 h of cyclic mechanical stretch exposure, mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. Activity is given as OD (optical density) change over time (mean ± s.d., n = 3). (C) siRNA knockdown of succinate-CoA ligase (SUCLG). RT PCR for SUCLG from A549 cells after siRNA treatment compared with control siRNA treatment (CsiR; beta-actin was used as house-keeping gene; n = 3). Note: siRNA knockdown revealed 82% reduction of SUCLG transcript. (D) A549 cells following siRNA repression of succinate-CoA ligase (siSUCLG) or treatment with nonspecific control siRNA (CsiR) were stretched for 0 or 8 h, lysed, and blotted for HIF1A. One representative blot of three is displayed. (E) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without α-ketoglutarate (aKG) treatment. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed. (F–H) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 h with or without inhibitors of JNK, ERK, or <t>p38.</t> Mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. (I) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without neutralizing antibodies for TNFA or IL-6. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed.
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Bayer AG bayer p38 kinase inhibitors
(A) Confluent Calu-3 cells underwent cyclic mechanical stretch for 24 h. Partial oxygen pressures (pO2) from supernatants were determined using I-STAT analyzer and compared to un-stretched controls (mean ± s.d., n = 3). (B) Following 8 or 24 h of cyclic mechanical stretch exposure, mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. Activity is given as OD (optical density) change over time (mean ± s.d., n = 3). (C) siRNA knockdown of succinate-CoA ligase (SUCLG). RT PCR for SUCLG from A549 cells after siRNA treatment compared with control siRNA treatment (CsiR; beta-actin was used as house-keeping gene; n = 3). Note: siRNA knockdown revealed 82% reduction of SUCLG transcript. (D) A549 cells following siRNA repression of succinate-CoA ligase (siSUCLG) or treatment with nonspecific control siRNA (CsiR) were stretched for 0 or 8 h, lysed, and blotted for HIF1A. One representative blot of three is displayed. (E) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without α-ketoglutarate (aKG) treatment. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed. (F–H) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 h with or without inhibitors of JNK, ERK, or <t>p38.</t> Mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. (I) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without neutralizing antibodies for TNFA or IL-6. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed.
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SangStat Inc rdp-58
(A) Confluent Calu-3 cells underwent cyclic mechanical stretch for 24 h. Partial oxygen pressures (pO2) from supernatants were determined using I-STAT analyzer and compared to un-stretched controls (mean ± s.d., n = 3). (B) Following 8 or 24 h of cyclic mechanical stretch exposure, mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. Activity is given as OD (optical density) change over time (mean ± s.d., n = 3). (C) siRNA knockdown of succinate-CoA ligase (SUCLG). RT PCR for SUCLG from A549 cells after siRNA treatment compared with control siRNA treatment (CsiR; beta-actin was used as house-keeping gene; n = 3). Note: siRNA knockdown revealed 82% reduction of SUCLG transcript. (D) A549 cells following siRNA repression of succinate-CoA ligase (siSUCLG) or treatment with nonspecific control siRNA (CsiR) were stretched for 0 or 8 h, lysed, and blotted for HIF1A. One representative blot of three is displayed. (E) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without α-ketoglutarate (aKG) treatment. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed. (F–H) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 h with or without inhibitors of JNK, ERK, or <t>p38.</t> Mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. (I) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without neutralizing antibodies for TNFA or IL-6. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed.
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90
Monsanto Technology LLC sc-040
(A) Confluent Calu-3 cells underwent cyclic mechanical stretch for 24 h. Partial oxygen pressures (pO2) from supernatants were determined using I-STAT analyzer and compared to un-stretched controls (mean ± s.d., n = 3). (B) Following 8 or 24 h of cyclic mechanical stretch exposure, mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. Activity is given as OD (optical density) change over time (mean ± s.d., n = 3). (C) siRNA knockdown of succinate-CoA ligase (SUCLG). RT PCR for SUCLG from A549 cells after siRNA treatment compared with control siRNA treatment (CsiR; beta-actin was used as house-keeping gene; n = 3). Note: siRNA knockdown revealed 82% reduction of SUCLG transcript. (D) A549 cells following siRNA repression of succinate-CoA ligase (siSUCLG) or treatment with nonspecific control siRNA (CsiR) were stretched for 0 or 8 h, lysed, and blotted for HIF1A. One representative blot of three is displayed. (E) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without α-ketoglutarate (aKG) treatment. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed. (F–H) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 h with or without inhibitors of JNK, ERK, or <t>p38.</t> Mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. (I) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without neutralizing antibodies for TNFA or IL-6. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed.
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Fujisawa Pharmaceutical Co Ltd fr-167653
(A) Confluent Calu-3 cells underwent cyclic mechanical stretch for 24 h. Partial oxygen pressures (pO2) from supernatants were determined using I-STAT analyzer and compared to un-stretched controls (mean ± s.d., n = 3). (B) Following 8 or 24 h of cyclic mechanical stretch exposure, mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. Activity is given as OD (optical density) change over time (mean ± s.d., n = 3). (C) siRNA knockdown of succinate-CoA ligase (SUCLG). RT PCR for SUCLG from A549 cells after siRNA treatment compared with control siRNA treatment (CsiR; beta-actin was used as house-keeping gene; n = 3). Note: siRNA knockdown revealed 82% reduction of SUCLG transcript. (D) A549 cells following siRNA repression of succinate-CoA ligase (siSUCLG) or treatment with nonspecific control siRNA (CsiR) were stretched for 0 or 8 h, lysed, and blotted for HIF1A. One representative blot of three is displayed. (E) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without α-ketoglutarate (aKG) treatment. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed. (F–H) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 h with or without inhibitors of JNK, ERK, or <t>p38.</t> Mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. (I) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without neutralizing antibodies for TNFA or IL-6. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed.
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Monsanto Technology LLC sc-xx906
(A) Confluent Calu-3 cells underwent cyclic mechanical stretch for 24 h. Partial oxygen pressures (pO2) from supernatants were determined using I-STAT analyzer and compared to un-stretched controls (mean ± s.d., n = 3). (B) Following 8 or 24 h of cyclic mechanical stretch exposure, mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. Activity is given as OD (optical density) change over time (mean ± s.d., n = 3). (C) siRNA knockdown of succinate-CoA ligase (SUCLG). RT PCR for SUCLG from A549 cells after siRNA treatment compared with control siRNA treatment (CsiR; beta-actin was used as house-keeping gene; n = 3). Note: siRNA knockdown revealed 82% reduction of SUCLG transcript. (D) A549 cells following siRNA repression of succinate-CoA ligase (siSUCLG) or treatment with nonspecific control siRNA (CsiR) were stretched for 0 or 8 h, lysed, and blotted for HIF1A. One representative blot of three is displayed. (E) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without α-ketoglutarate (aKG) treatment. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed. (F–H) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 h with or without inhibitors of JNK, ERK, or <t>p38.</t> Mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. (I) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without neutralizing antibodies for TNFA or IL-6. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed.
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Scios Inc scios-323
(A) Confluent Calu-3 cells underwent cyclic mechanical stretch for 24 h. Partial oxygen pressures (pO2) from supernatants were determined using I-STAT analyzer and compared to un-stretched controls (mean ± s.d., n = 3). (B) Following 8 or 24 h of cyclic mechanical stretch exposure, mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. Activity is given as OD (optical density) change over time (mean ± s.d., n = 3). (C) siRNA knockdown of succinate-CoA ligase (SUCLG). RT PCR for SUCLG from A549 cells after siRNA treatment compared with control siRNA treatment (CsiR; beta-actin was used as house-keeping gene; n = 3). Note: siRNA knockdown revealed 82% reduction of SUCLG transcript. (D) A549 cells following siRNA repression of succinate-CoA ligase (siSUCLG) or treatment with nonspecific control siRNA (CsiR) were stretched for 0 or 8 h, lysed, and blotted for HIF1A. One representative blot of three is displayed. (E) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without α-ketoglutarate (aKG) treatment. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed. (F–H) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 h with or without inhibitors of JNK, ERK, or <t>p38.</t> Mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. (I) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without neutralizing antibodies for TNFA or IL-6. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed.
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LEO Pharma leo map kinase inhibitors
(A) Confluent Calu-3 cells underwent cyclic mechanical stretch for 24 h. Partial oxygen pressures (pO2) from supernatants were determined using I-STAT analyzer and compared to un-stretched controls (mean ± s.d., n = 3). (B) Following 8 or 24 h of cyclic mechanical stretch exposure, mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. Activity is given as OD (optical density) change over time (mean ± s.d., n = 3). (C) siRNA knockdown of succinate-CoA ligase (SUCLG). RT PCR for SUCLG from A549 cells after siRNA treatment compared with control siRNA treatment (CsiR; beta-actin was used as house-keeping gene; n = 3). Note: siRNA knockdown revealed 82% reduction of SUCLG transcript. (D) A549 cells following siRNA repression of succinate-CoA ligase (siSUCLG) or treatment with nonspecific control siRNA (CsiR) were stretched for 0 or 8 h, lysed, and blotted for HIF1A. One representative blot of three is displayed. (E) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without α-ketoglutarate (aKG) treatment. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed. (F–H) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 h with or without inhibitors of JNK, ERK, or <t>p38.</t> Mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. (I) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without neutralizing antibodies for TNFA or IL-6. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed.
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Signal Research mkk3/mkk6 inhibitors
(A) Confluent Calu-3 cells underwent cyclic mechanical stretch for 24 h. Partial oxygen pressures (pO2) from supernatants were determined using I-STAT analyzer and compared to un-stretched controls (mean ± s.d., n = 3). (B) Following 8 or 24 h of cyclic mechanical stretch exposure, mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. Activity is given as OD (optical density) change over time (mean ± s.d., n = 3). (C) siRNA knockdown of succinate-CoA ligase (SUCLG). RT PCR for SUCLG from A549 cells after siRNA treatment compared with control siRNA treatment (CsiR; beta-actin was used as house-keeping gene; n = 3). Note: siRNA knockdown revealed 82% reduction of SUCLG transcript. (D) A549 cells following siRNA repression of succinate-CoA ligase (siSUCLG) or treatment with nonspecific control siRNA (CsiR) were stretched for 0 or 8 h, lysed, and blotted for HIF1A. One representative blot of three is displayed. (E) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without α-ketoglutarate (aKG) treatment. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed. (F–H) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 h with or without inhibitors of JNK, ERK, or <t>p38.</t> Mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. (I) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without neutralizing antibodies for TNFA or IL-6. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed.
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Signal Research p38/mek modulators
(A) Confluent Calu-3 cells underwent cyclic mechanical stretch for 24 h. Partial oxygen pressures (pO2) from supernatants were determined using I-STAT analyzer and compared to un-stretched controls (mean ± s.d., n = 3). (B) Following 8 or 24 h of cyclic mechanical stretch exposure, mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. Activity is given as OD (optical density) change over time (mean ± s.d., n = 3). (C) siRNA knockdown of succinate-CoA ligase (SUCLG). RT PCR for SUCLG from A549 cells after siRNA treatment compared with control siRNA treatment (CsiR; beta-actin was used as house-keeping gene; n = 3). Note: siRNA knockdown revealed 82% reduction of SUCLG transcript. (D) A549 cells following siRNA repression of succinate-CoA ligase (siSUCLG) or treatment with nonspecific control siRNA (CsiR) were stretched for 0 or 8 h, lysed, and blotted for HIF1A. One representative blot of three is displayed. (E) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without α-ketoglutarate (aKG) treatment. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed. (F–H) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 h with or without inhibitors of JNK, ERK, or <t>p38.</t> Mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. (I) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without neutralizing antibodies for TNFA or IL-6. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed.
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(A) Confluent Calu-3 cells underwent cyclic mechanical stretch for 24 h. Partial oxygen pressures (pO2) from supernatants were determined using I-STAT analyzer and compared to un-stretched controls (mean ± s.d., n = 3). (B) Following 8 or 24 h of cyclic mechanical stretch exposure, mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. Activity is given as OD (optical density) change over time (mean ± s.d., n = 3). (C) siRNA knockdown of succinate-CoA ligase (SUCLG). RT PCR for SUCLG from A549 cells after siRNA treatment compared with control siRNA treatment (CsiR; beta-actin was used as house-keeping gene; n = 3). Note: siRNA knockdown revealed 82% reduction of SUCLG transcript. (D) A549 cells following siRNA repression of succinate-CoA ligase (siSUCLG) or treatment with nonspecific control siRNA (CsiR) were stretched for 0 or 8 h, lysed, and blotted for HIF1A. One representative blot of three is displayed. (E) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without α-ketoglutarate (aKG) treatment. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed. (F–H) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 h with or without inhibitors of JNK, ERK, or p38. Mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. (I) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without neutralizing antibodies for TNFA or IL-6. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed.

Journal: PLoS Biology

Article Title: HIF1A Reduces Acute Lung Injury by Optimizing Carbohydrate Metabolism in the Alveolar Epithelium

doi: 10.1371/journal.pbio.1001665

Figure Lengend Snippet: (A) Confluent Calu-3 cells underwent cyclic mechanical stretch for 24 h. Partial oxygen pressures (pO2) from supernatants were determined using I-STAT analyzer and compared to un-stretched controls (mean ± s.d., n = 3). (B) Following 8 or 24 h of cyclic mechanical stretch exposure, mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. Activity is given as OD (optical density) change over time (mean ± s.d., n = 3). (C) siRNA knockdown of succinate-CoA ligase (SUCLG). RT PCR for SUCLG from A549 cells after siRNA treatment compared with control siRNA treatment (CsiR; beta-actin was used as house-keeping gene; n = 3). Note: siRNA knockdown revealed 82% reduction of SUCLG transcript. (D) A549 cells following siRNA repression of succinate-CoA ligase (siSUCLG) or treatment with nonspecific control siRNA (CsiR) were stretched for 0 or 8 h, lysed, and blotted for HIF1A. One representative blot of three is displayed. (E) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without α-ketoglutarate (aKG) treatment. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed. (F–H) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 h with or without inhibitors of JNK, ERK, or p38. Mitochondrial fractions of Calu-3 cells were obtained and analyzed for succinate dehydrogenase (SDH, mitochondrial Complex II) activity using ELISA. (I) Confluent Calu-3 cells underwent cyclic mechanical stretch for 8 or 24 h with and without neutralizing antibodies for TNFA or IL-6. Cells were lysed and blotted for HIF1A. One representative blot of three is displayed.

Article Snippet: To inhibit MAP kinases in vitro , AMG 548 [Tocris, potent and selective inhibitor of p38 (at 10 μM inhibits p38α, p38β, p38γ, and p38δ)], FR 180204 [Tocris, selective ERK inhibitor (at 1 μM inhibits ERK2 and ERK1)], and BI 78D3 [Tocris, competitive c-Jun N-terminal kinase (JNK) inhibitor (500 nM)] was used.

Techniques: Activity Assay, Enzyme-linked Immunosorbent Assay, Knockdown, Reverse Transcription Polymerase Chain Reaction, Control