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10.1038/srep36544 http://scihub22266oqcxt.onion/10.1038/srep36544 C5109916!5109916 !27811956     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27811956 &cmd=llinks): Failed to open stream: HTTP request failed! 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Probing the PI3K/Akt/mTor pathway using (31)P-NMR spectroscopy: routes to glycogen synthase kinase 3 |pdf=|usr=}}{{27811956 }} gab.com Text Probing the PI3K/Akt/mTor pathway using (31)P-NMR spectroscopy: routes to glycogen synthase kinase 3 JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27811956 #FOAvip Akt is an intracellular signalling pathway that serves as an essential link between cell surface receptors and cellular processes including proliferation, development and survival. The pathway has many downstream targets including glycogen synthase kinase3 which is a major regulatory kinase for cell cycle transit as well as controlling glycogen synthase activity. The Akt pathway is frequently up-regulated in cancer due to overexpression of receptors such as the epidermal growth factor receptor, or mutation of signalling pathway kinases resulting in inappropriate survival and proliferation. Consequently anticancer drugs have been developed that target this pathway. MDA-MB-468 breast and HCT8 colorectal cancer cells were treated with inhibitors including LY294002, MK2206, rapamycin, AZD8055 targeting key kinases in/associated with Akt pathway and the consistency of changes in (31)P-NMR-detecatable metabolite content of tumour cells was examined. Treatment with the Akt inhibitor MK2206 reduced phosphocholine levels in MDA-MB-468 cells. Treatment with either the phosphoinositide-3-kinase inhibitor, LY294002 and pan-mTOR inhibitor, AZD8055 but not pan-Akt inhibitor MK2206 increased uridine-5'-diphosphate-hexose cell content which was suppressed by co-treatment with glycogen synthase kinase 3 inhibitor SB216763. This suggests that there is an Akt-independent link between phosphoinositol-3-kinase and glycogen synthase kinase3 and demonstrates the potential of (31)P-NMR to probe intracellular signalling pathways. Twit Text FOAVip Probing the PI3K/Akt/mTor pathway using (31)P-NMR spectroscopy: routes to glycogen synthase kinase 3 ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27811956 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27811956 #FOAvip English Wikipedia <ref>{{Cite pmid|27811956 }}</ref> Probing the PI3K/Akt/mTor pathway using (31)P-NMR spectroscopy: routes to glycogen synthase kinase 3 #MMPMID27811956 Phyu SM ; Tseng CC ; Fleming IN ; Smith TA Sci Rep 2016[Nov]; 6 (ä): 36544 PMID27811956 show ga Akt is an intracellular signalling pathway that serves as an essential link between cell surface receptors and cellular processes including proliferation, development and survival. The pathway has many downstream targets including glycogen synthase kinase3 which is a major regulatory kinase for cell cycle transit as well as controlling glycogen synthase activity. The Akt pathway is frequently up-regulated in cancer due to overexpression of receptors such as the epidermal growth factor receptor, or mutation of signalling pathway kinases resulting in inappropriate survival and proliferation. Consequently anticancer drugs have been developed that target this pathway. MDA-MB-468 breast and HCT8 colorectal cancer cells were treated with inhibitors including LY294002, MK2206, rapamycin, AZD8055 targeting key kinases in/associated with Akt pathway and the consistency of changes in (31)P-NMR-detecatable metabolite content of tumour cells was examined. Treatment with the Akt inhibitor MK2206 reduced phosphocholine levels in MDA-MB-468 cells. Treatment with either the phosphoinositide-3-kinase inhibitor, LY294002 and pan-mTOR inhibitor, AZD8055 but not pan-Akt inhibitor MK2206 increased uridine-5'-diphosphate-hexose cell content which was suppressed by co-treatment with glycogen synthase kinase 3 inhibitor SB216763. This suggests that there is an Akt-independent link between phosphoinositol-3-kinase and glycogen synthase kinase3 and demonstrates the potential of (31)P-NMR to probe intracellular signalling pathways. |Antineoplastic Agents/pharmacology [MESH] |Apoptosis/drug effects [MESH] |Cell Cycle/drug effects [MESH] |Cell Line, Tumor [MESH] |Cell Proliferation/drug effects [MESH] |Chromones/pharmacology [MESH] |ErbB Receptors/metabolism [MESH] |Glycogen Synthase Kinase 3/*metabolism [MESH] |Heterocyclic Compounds, 3-Ring/pharmacology [MESH] |Humans [MESH] |Magnetic Resonance Spectroscopy/methods [MESH] |Morpholines/pharmacology [MESH] |Phosphatidylinositol 3-Kinases/*metabolism [MESH] |Phosphoinositide-3 Kinase Inhibitors [MESH] |Phosphorylation/drug effects/physiology [MESH] |Protein Kinase Inhibitors/pharmacology [MESH] |Proto-Oncogene Proteins c-akt/antagonists & inhibitors/*metabolism [MESH] |Signal Transduction/drug effects/physiology [MESH]Probing the PI3K/Akt/mTor pathway using (31)P-NMR spectroscopy: routes(epmc).pdf DeepDyve Pubget Overpricing