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10.1016/j.cell.2014.11.020 http://scihub22266oqcxt.onion/10.1016/j.cell.2014.11.020 C4272450!4272450 !25525877     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25525877 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25525877 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cell 2014 ; 159 (7 ): 1591-602 Nephropedia Template TP {{tp|p=25525877 |t=2014. Acetate dependence of tumors |pdf=|usr=}}{{25525877 }} gab.com Text Acetate dependence of tumors JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=25525877 #FOAvip Acetyl-CoA represents a central node of carbon metabolism that plays a key role in bioenergetics, cell proliferation, and the regulation of gene expression. Highly glycolytic or hypoxic tumors must produce sufficient quantities of this metabolite to support cell growth and survival under nutrient-limiting conditions. Here, we show that the nucleocytosolic acetyl-CoA synthetase enzyme, ACSS2, supplies a key source of acetyl-CoA for tumors by capturing acetate as a carbon source. Despite exhibiting no gross deficits in growth or development, adult mice lacking ACSS2 exhibit a significant reduction in tumor burden in two different models of hepatocellular carcinoma. ACSS2 is expressed in a large proportion of human tumors, and its activity is responsible for the majority of cellular acetate uptake into both lipids and histones. These observations may qualify ACSS2 as a targetable metabolic vulnerability of a wide spectrum of tumors. Twit Text FOAVip Acetate dependence of tumors ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=25525877 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25525877 #FOAvip English Wikipedia <ref>{{Cite pmid|25525877 }}</ref> Acetate dependence of tumors #MMPMID25525877 Comerford SA ; Huang Z ; Du X ; Wang Y ; Cai L ; Witkiewicz AK ; Walters H ; Tantawy MN ; Fu A ; Manning HC ; Horton JD ; Hammer RE ; McKnight SL ; Tu BP Cell 2014[Dec]; 159 (7 ): 1591-602 PMID25525877 show ga Acetyl-CoA represents a central node of carbon metabolism that plays a key role in bioenergetics, cell proliferation, and the regulation of gene expression. Highly glycolytic or hypoxic tumors must produce sufficient quantities of this metabolite to support cell growth and survival under nutrient-limiting conditions. Here, we show that the nucleocytosolic acetyl-CoA synthetase enzyme, ACSS2, supplies a key source of acetyl-CoA for tumors by capturing acetate as a carbon source. Despite exhibiting no gross deficits in growth or development, adult mice lacking ACSS2 exhibit a significant reduction in tumor burden in two different models of hepatocellular carcinoma. ACSS2 is expressed in a large proportion of human tumors, and its activity is responsible for the majority of cellular acetate uptake into both lipids and histones. These observations may qualify ACSS2 as a targetable metabolic vulnerability of a wide spectrum of tumors. |Acetate-CoA Ligase/analysis/genetics/*metabolism [MESH] |Acetates/*metabolism [MESH] |Acetyl Coenzyme A/metabolism [MESH] |Animals [MESH] |Humans [MESH] |Immunohistochemistry [MESH] |Liver Neoplasms/metabolism [MESH] |Mice [MESH] |Neoplasms/chemistry/*metabolism/pathology [MESH] |Positron-Emission Tomography [MESH]Acetate dependence of tumors (epmc).pdf DeepDyve Pubget Overpricing