akt pathway inhibitor mk2206 Search Results


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Selleck Chemicals akt inhibitor
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Selleck Chemicals akt inhibitor mk2206 2hcl
PI3K/AKT and JNK/c-Jun pathway facilitated by Quisinostat were required for cell cycle arrest and cell apoptosis. (A) HCCLM3 and SMMC-7721 cells were treated with quisinostat (12.5, 25.0 and 50.0nM) for 48 h. Western blot analysis was used to evaluate expressions of PI3K-p110, PI3K-p85, phosphorylation of AKT 473 , JNK, phosphorylation of JNK and c-Jun. Data, mean ± SD (n = 3); *, P < 0.05; **, P < 0.01 compared with DMSO group. (B) Cells were preincubated for 5 h with or without <t>MK2206</t> <t>2HCL(5μM),</t> followed by culturing with 25nM quisinostat for 48 h, then conducting the cell cycle analysis and (C) Expression levels of phosphorylation of AKT 473 and p21 proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *, P < 0.05; **, P < 0.01; ***, P < 0.001 compared with the DMSO group. (D) Cells were pretreated with or without 40μM Z-VAD-FMK for 2 h, followed by culturing with 25nM quisinostat for 48 h to conduct apoptosis analysis, (E) cell proliferation analysis and (F) Expression levels of cle-Caspase9, cle-Caspase3, PARP, and cle-PARP proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *P <0.05; **P < 0.01; ***P < 0.001 compared with Quisinostat group. (G) Cells were pretreated with SP600125 (6μM) for 5 h followed by culturing with 25nM quisinostat for 48 h to conduct apoptosis analysis, (H) cell proliferation analysis and (I) Expression levels of phosphorylation of JNK, cle-Caspase3 and cle-PARP proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *P <0.05; **P < 0.01; ***P < 0.001 compared with Quisinostat group.
Akt Inhibitor Mk2206 2hcl, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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PI3K/AKT and JNK/c-Jun pathway facilitated by Quisinostat were required for cell cycle arrest and cell apoptosis. (A) HCCLM3 and SMMC-7721 cells were treated with quisinostat (12.5, 25.0 and 50.0nM) for 48 h. Western blot analysis was used to evaluate expressions of PI3K-p110, PI3K-p85, phosphorylation of AKT 473 , JNK, phosphorylation of JNK and c-Jun. Data, mean ± SD (n = 3); *, P < 0.05; **, P < 0.01 compared with DMSO group. (B) Cells were preincubated for 5 h with or without <t>MK2206</t> <t>2HCL(5μM),</t> followed by culturing with 25nM quisinostat for 48 h, then conducting the cell cycle analysis and (C) Expression levels of phosphorylation of AKT 473 and p21 proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *, P < 0.05; **, P < 0.01; ***, P < 0.001 compared with the DMSO group. (D) Cells were pretreated with or without 40μM Z-VAD-FMK for 2 h, followed by culturing with 25nM quisinostat for 48 h to conduct apoptosis analysis, (E) cell proliferation analysis and (F) Expression levels of cle-Caspase9, cle-Caspase3, PARP, and cle-PARP proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *P <0.05; **P < 0.01; ***P < 0.001 compared with Quisinostat group. (G) Cells were pretreated with SP600125 (6μM) for 5 h followed by culturing with 25nM quisinostat for 48 h to conduct apoptosis analysis, (H) cell proliferation analysis and (I) Expression levels of phosphorylation of JNK, cle-Caspase3 and cle-PARP proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *P <0.05; **P < 0.01; ***P < 0.001 compared with Quisinostat group.
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Beyotime akt inhibitor mk-2206
PI3K/AKT and JNK/c-Jun pathway facilitated by Quisinostat were required for cell cycle arrest and cell apoptosis. (A) HCCLM3 and SMMC-7721 cells were treated with quisinostat (12.5, 25.0 and 50.0nM) for 48 h. Western blot analysis was used to evaluate expressions of PI3K-p110, PI3K-p85, phosphorylation of AKT 473 , JNK, phosphorylation of JNK and c-Jun. Data, mean ± SD (n = 3); *, P < 0.05; **, P < 0.01 compared with DMSO group. (B) Cells were preincubated for 5 h with or without <t>MK2206</t> <t>2HCL(5μM),</t> followed by culturing with 25nM quisinostat for 48 h, then conducting the cell cycle analysis and (C) Expression levels of phosphorylation of AKT 473 and p21 proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *, P < 0.05; **, P < 0.01; ***, P < 0.001 compared with the DMSO group. (D) Cells were pretreated with or without 40μM Z-VAD-FMK for 2 h, followed by culturing with 25nM quisinostat for 48 h to conduct apoptosis analysis, (E) cell proliferation analysis and (F) Expression levels of cle-Caspase9, cle-Caspase3, PARP, and cle-PARP proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *P <0.05; **P < 0.01; ***P < 0.001 compared with Quisinostat group. (G) Cells were pretreated with SP600125 (6μM) for 5 h followed by culturing with 25nM quisinostat for 48 h to conduct apoptosis analysis, (H) cell proliferation analysis and (I) Expression levels of phosphorylation of JNK, cle-Caspase3 and cle-PARP proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *P <0.05; **P < 0.01; ***P < 0.001 compared with Quisinostat group.
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Cayman Chemical mk-2206 2hcl
PI3K/AKT and JNK/c-Jun pathway facilitated by Quisinostat were required for cell cycle arrest and cell apoptosis. (A) HCCLM3 and SMMC-7721 cells were treated with quisinostat (12.5, 25.0 and 50.0nM) for 48 h. Western blot analysis was used to evaluate expressions of PI3K-p110, PI3K-p85, phosphorylation of AKT 473 , JNK, phosphorylation of JNK and c-Jun. Data, mean ± SD (n = 3); *, P < 0.05; **, P < 0.01 compared with DMSO group. (B) Cells were preincubated for 5 h with or without <t>MK2206</t> <t>2HCL(5μM),</t> followed by culturing with 25nM quisinostat for 48 h, then conducting the cell cycle analysis and (C) Expression levels of phosphorylation of AKT 473 and p21 proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *, P < 0.05; **, P < 0.01; ***, P < 0.001 compared with the DMSO group. (D) Cells were pretreated with or without 40μM Z-VAD-FMK for 2 h, followed by culturing with 25nM quisinostat for 48 h to conduct apoptosis analysis, (E) cell proliferation analysis and (F) Expression levels of cle-Caspase9, cle-Caspase3, PARP, and cle-PARP proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *P <0.05; **P < 0.01; ***P < 0.001 compared with Quisinostat group. (G) Cells were pretreated with SP600125 (6μM) for 5 h followed by culturing with 25nM quisinostat for 48 h to conduct apoptosis analysis, (H) cell proliferation analysis and (I) Expression levels of phosphorylation of JNK, cle-Caspase3 and cle-PARP proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *P <0.05; **P < 0.01; ***P < 0.001 compared with Quisinostat group.
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PI3K/AKT and JNK/c-Jun pathway facilitated by Quisinostat were required for cell cycle arrest and cell apoptosis. (A) HCCLM3 and SMMC-7721 cells were treated with quisinostat (12.5, 25.0 and 50.0nM) for 48 h. Western blot analysis was used to evaluate expressions of PI3K-p110, PI3K-p85, phosphorylation of AKT 473 , JNK, phosphorylation of JNK and c-Jun. Data, mean ± SD (n = 3); *, P < 0.05; **, P < 0.01 compared with DMSO group. (B) Cells were preincubated for 5 h with or without MK2206 2HCL(5μM), followed by culturing with 25nM quisinostat for 48 h, then conducting the cell cycle analysis and (C) Expression levels of phosphorylation of AKT 473 and p21 proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *, P < 0.05; **, P < 0.01; ***, P < 0.001 compared with the DMSO group. (D) Cells were pretreated with or without 40μM Z-VAD-FMK for 2 h, followed by culturing with 25nM quisinostat for 48 h to conduct apoptosis analysis, (E) cell proliferation analysis and (F) Expression levels of cle-Caspase9, cle-Caspase3, PARP, and cle-PARP proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *P <0.05; **P < 0.01; ***P < 0.001 compared with Quisinostat group. (G) Cells were pretreated with SP600125 (6μM) for 5 h followed by culturing with 25nM quisinostat for 48 h to conduct apoptosis analysis, (H) cell proliferation analysis and (I) Expression levels of phosphorylation of JNK, cle-Caspase3 and cle-PARP proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *P <0.05; **P < 0.01; ***P < 0.001 compared with Quisinostat group.

Journal: International Journal of Biological Sciences

Article Title: The HDAC Inhibitor Quisinostat (JNJ-26481585) Supresses Hepatocellular Carcinoma alone and Synergistically in Combination with Sorafenib by G0/G1 phase arrest and Apoptosis induction

doi: 10.7150/ijbs.27661

Figure Lengend Snippet: PI3K/AKT and JNK/c-Jun pathway facilitated by Quisinostat were required for cell cycle arrest and cell apoptosis. (A) HCCLM3 and SMMC-7721 cells were treated with quisinostat (12.5, 25.0 and 50.0nM) for 48 h. Western blot analysis was used to evaluate expressions of PI3K-p110, PI3K-p85, phosphorylation of AKT 473 , JNK, phosphorylation of JNK and c-Jun. Data, mean ± SD (n = 3); *, P < 0.05; **, P < 0.01 compared with DMSO group. (B) Cells were preincubated for 5 h with or without MK2206 2HCL(5μM), followed by culturing with 25nM quisinostat for 48 h, then conducting the cell cycle analysis and (C) Expression levels of phosphorylation of AKT 473 and p21 proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *, P < 0.05; **, P < 0.01; ***, P < 0.001 compared with the DMSO group. (D) Cells were pretreated with or without 40μM Z-VAD-FMK for 2 h, followed by culturing with 25nM quisinostat for 48 h to conduct apoptosis analysis, (E) cell proliferation analysis and (F) Expression levels of cle-Caspase9, cle-Caspase3, PARP, and cle-PARP proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *P <0.05; **P < 0.01; ***P < 0.001 compared with Quisinostat group. (G) Cells were pretreated with SP600125 (6μM) for 5 h followed by culturing with 25nM quisinostat for 48 h to conduct apoptosis analysis, (H) cell proliferation analysis and (I) Expression levels of phosphorylation of JNK, cle-Caspase3 and cle-PARP proteins were detected by Western Blotting. Data were shown as mean ± SD. n = 3; *P <0.05; **P < 0.01; ***P < 0.001 compared with Quisinostat group.

Article Snippet: Sorafenib, quisinostat (JNJ-26481585), JNK inhibitor SP600125, AKT inhibitor MK2206 2HCL and Caspase inhibitor Z-VAD-FMK were from Selleckchem (Houston, Texas, USA).

Techniques: Western Blot, Phospho-proteomics, Cell Cycle Assay, Expressing