p akt inhibitor mk2206 Search Results


mk 2206 3 methyladenine 3 ma  (MedChemExpress)
96
MedChemExpress mk 2206 3 methyladenine 3 ma
Mk 2206 3 Methyladenine 3 Ma, supplied by MedChemExpress, 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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mk2206  (Adooq Bioscience LLC)
90
Adooq Bioscience LLC mk2206
(A-C) Control and GNPNAT1 KO 22Rv1 cell lysate samples were Western blot-analyzed for the levels of AKT and its phosphorylated form p-AKT (A) as well as AKT downstream signaling pathways including components of the mTOR pathway (B), and the PKC pathway (C). (D-E) Microscopic images (D) and cell proliferation assay (E) after treating control and GNPNAT1 KO with the AKT inhibitor, <t>MK2206</t> after 48 h. Scale bars, 200 µm. F) Cell proliferation assay after treatment with UDP-GlcNAc after 48 h. (G) Cell proliferation assay after pre-treatment with 10 µM MK2206 followed by co-treatment with 10 µM MK2206 and 30 µM UDP-GlcNAc or UDP-GlcNAc alone. (H) Schematic diagram of the possible mechanism for increased cell proliferation in GNPNAT1 KO cells, via the alteration of AKT and its downstream signaling pathways.
Mk2206, supplied by Adooq Bioscience LLC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mk2206  (SAS institute)
90
SAS institute mk2206
(A-C) Control and GNPNAT1 KO 22Rv1 cell lysate samples were Western blot-analyzed for the levels of AKT and its phosphorylated form p-AKT (A) as well as AKT downstream signaling pathways including components of the mTOR pathway (B), and the PKC pathway (C). (D-E) Microscopic images (D) and cell proliferation assay (E) after treating control and GNPNAT1 KO with the AKT inhibitor, <t>MK2206</t> after 48 h. Scale bars, 200 µm. F) Cell proliferation assay after treatment with UDP-GlcNAc after 48 h. (G) Cell proliferation assay after pre-treatment with 10 µM MK2206 followed by co-treatment with 10 µM MK2206 and 30 µM UDP-GlcNAc or UDP-GlcNAc alone. (H) Schematic diagram of the possible mechanism for increased cell proliferation in GNPNAT1 KO cells, via the alteration of AKT and its downstream signaling pathways.
Mk2206, supplied by SAS institute, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
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mk2206  (Selleck Chemicals)
96
Selleck Chemicals mk2206
(A-C) Control and GNPNAT1 KO 22Rv1 cell lysate samples were Western blot-analyzed for the levels of AKT and its phosphorylated form p-AKT (A) as well as AKT downstream signaling pathways including components of the mTOR pathway (B), and the PKC pathway (C). (D-E) Microscopic images (D) and cell proliferation assay (E) after treating control and GNPNAT1 KO with the AKT inhibitor, <t>MK2206</t> after 48 h. Scale bars, 200 µm. F) Cell proliferation assay after treatment with UDP-GlcNAc after 48 h. (G) Cell proliferation assay after pre-treatment with 10 µM MK2206 followed by co-treatment with 10 µM MK2206 and 30 µM UDP-GlcNAc or UDP-GlcNAc alone. (H) Schematic diagram of the possible mechanism for increased cell proliferation in GNPNAT1 KO cells, via the alteration of AKT and its downstream signaling pathways.
Mk2206, 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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mk 2206  (Selleck Chemicals)
94
Selleck Chemicals mk 2206
(A-C) Control and GNPNAT1 KO 22Rv1 cell lysate samples were Western blot-analyzed for the levels of AKT and its phosphorylated form p-AKT (A) as well as AKT downstream signaling pathways including components of the mTOR pathway (B), and the PKC pathway (C). (D-E) Microscopic images (D) and cell proliferation assay (E) after treating control and GNPNAT1 KO with the AKT inhibitor, <t>MK2206</t> after 48 h. Scale bars, 200 µm. F) Cell proliferation assay after treatment with UDP-GlcNAc after 48 h. (G) Cell proliferation assay after pre-treatment with 10 µM MK2206 followed by co-treatment with 10 µM MK2206 and 30 µM UDP-GlcNAc or UDP-GlcNAc alone. (H) Schematic diagram of the possible mechanism for increased cell proliferation in GNPNAT1 KO cells, via the alteration of AKT and its downstream signaling pathways.
Mk 2206, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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akt  (Selleck Chemicals)
96
Selleck Chemicals akt
(A-C) Control and GNPNAT1 KO 22Rv1 cell lysate samples were Western blot-analyzed for the levels of AKT and its phosphorylated form p-AKT (A) as well as AKT downstream signaling pathways including components of the mTOR pathway (B), and the PKC pathway (C). (D-E) Microscopic images (D) and cell proliferation assay (E) after treating control and GNPNAT1 KO with the AKT inhibitor, <t>MK2206</t> after 48 h. Scale bars, 200 µm. F) Cell proliferation assay after treatment with UDP-GlcNAc after 48 h. (G) Cell proliferation assay after pre-treatment with 10 µM MK2206 followed by co-treatment with 10 µM MK2206 and 30 µM UDP-GlcNAc or UDP-GlcNAc alone. (H) Schematic diagram of the possible mechanism for increased cell proliferation in GNPNAT1 KO cells, via the alteration of AKT and its downstream signaling pathways.
Akt, 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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akt - by Bioz Stars, 2026-02
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akt inhibitor  (Selleck Chemicals)
93
Selleck Chemicals akt inhibitor
(A-C) Control and GNPNAT1 KO 22Rv1 cell lysate samples were Western blot-analyzed for the levels of AKT and its phosphorylated form p-AKT (A) as well as AKT downstream signaling pathways including components of the mTOR pathway (B), and the PKC pathway (C). (D-E) Microscopic images (D) and cell proliferation assay (E) after treating control and GNPNAT1 KO with the AKT inhibitor, <t>MK2206</t> after 48 h. Scale bars, 200 µm. F) Cell proliferation assay after treatment with UDP-GlcNAc after 48 h. (G) Cell proliferation assay after pre-treatment with 10 µM MK2206 followed by co-treatment with 10 µM MK2206 and 30 µM UDP-GlcNAc or UDP-GlcNAc alone. (H) Schematic diagram of the possible mechanism for increased cell proliferation in GNPNAT1 KO cells, via the alteration of AKT and its downstream signaling pathways.
Akt Inhibitor, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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akt inhibitor mk2206 2hcl  (Selleck Chemicals)
96
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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akt selective inhibitor mk2206  (Selleck Chemicals)
93
Selleck Chemicals akt selective inhibitor mk2206
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 Selective Inhibitor Mk2206, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mk2206  (MedChemExpress)
96
MedChemExpress mk2206
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.
Mk2206, supplied by MedChemExpress, 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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mk-2206  (MedChemExpress)
96
MedChemExpress 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.
Mk 2206, supplied by MedChemExpress, 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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Image Search Results


(A-C) Control and GNPNAT1 KO 22Rv1 cell lysate samples were Western blot-analyzed for the levels of AKT and its phosphorylated form p-AKT (A) as well as AKT downstream signaling pathways including components of the mTOR pathway (B), and the PKC pathway (C). (D-E) Microscopic images (D) and cell proliferation assay (E) after treating control and GNPNAT1 KO with the AKT inhibitor, MK2206 after 48 h. Scale bars, 200 µm. F) Cell proliferation assay after treatment with UDP-GlcNAc after 48 h. (G) Cell proliferation assay after pre-treatment with 10 µM MK2206 followed by co-treatment with 10 µM MK2206 and 30 µM UDP-GlcNAc or UDP-GlcNAc alone. (H) Schematic diagram of the possible mechanism for increased cell proliferation in GNPNAT1 KO cells, via the alteration of AKT and its downstream signaling pathways.

Journal: bioRxiv

Article Title: The Hexosamine Biosynthetic Pathway alters the cytoskeleton to modulate cell proliferation and migration in metastatic prostate cancer

doi: 10.1101/2024.10.14.618283

Figure Lengend Snippet: (A-C) Control and GNPNAT1 KO 22Rv1 cell lysate samples were Western blot-analyzed for the levels of AKT and its phosphorylated form p-AKT (A) as well as AKT downstream signaling pathways including components of the mTOR pathway (B), and the PKC pathway (C). (D-E) Microscopic images (D) and cell proliferation assay (E) after treating control and GNPNAT1 KO with the AKT inhibitor, MK2206 after 48 h. Scale bars, 200 µm. F) Cell proliferation assay after treatment with UDP-GlcNAc after 48 h. (G) Cell proliferation assay after pre-treatment with 10 µM MK2206 followed by co-treatment with 10 µM MK2206 and 30 µM UDP-GlcNAc or UDP-GlcNAc alone. (H) Schematic diagram of the possible mechanism for increased cell proliferation in GNPNAT1 KO cells, via the alteration of AKT and its downstream signaling pathways.

Article Snippet: MK2206 was purchased from AdooQ Bioscience (Irvine, CA) and UDP-GlcNAc from Millipore sigma (Burlington, MA).

Techniques: Control, Western Blot, Proliferation Assay

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