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10.1038/onc.2015.453 http://scihub22266oqcxt.onion/10.1038/onc.2015.453 C4956508!4956508 !26973245     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26973245 &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 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26973245 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Oncogene 2016 ; 35 (29 ): 3829-38 Nephropedia Template TP {{tp|p=26973245 |t=2016. TAK1 regulates hepatic lipid homeostasis through SREBP |pdf=|usr=}}{{26973245 }} gab.com Text TAK1 regulates hepatic lipid homeostasis through SREBP JO: Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=26973245 #FOAvip Sterol-regulatory element-binding proteins (SREBPs) are key transcription factors regulating cholesterol and fatty acid biosynthesis. SREBP activity is tightly regulated to maintain lipid homeostasis, and is modulated upon extracellular stimuli such as growth factors. While the homeostatic SREBP regulation is well studied, stimuli-dependent regulatory mechanisms are still elusive. Here we demonstrate that SREBPs are regulated by a previously uncharacterized mechanism through transforming growth factor-? activated kinase 1 (TAK1), a signaling molecule of inflammation. We found that TAK1 binds to and inhibits mature forms of SREBPs. In an in vivo setting, hepatocyte-specific Tak1 deletion upregulates liver lipid deposition and lipogenic enzymes in the mouse model. Furthermore, hepatic Tak1 deficiency causes steatosis pathologies including elevated blood triglyceride and cholesterol levels, which are established risk factors for the development of hepatocellular carcinoma (HCC) and are indeed correlated with Tak1-deficiency-induced HCC development. Pharmacological inhibition of SREBPs alleviated the steatosis and reduced the expression level of the HCC marker gene in the Tak1-deficient liver. Thus, TAK1 regulation of SREBP critically contributes to the maintenance of liver homeostasis to prevent steatosis, which is a potentially important mechanism to prevent HCC development. Twit Text FOAVip TAK1 regulates hepatic lipid homeostasis through SREBP ????Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=26973245 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26973245 #FOAvip English Wikipedia <ref>{{Cite pmid|26973245 }}</ref> TAK1 regulates hepatic lipid homeostasis through SREBP #MMPMID26973245 Morioka S ; Sai K ; Omori E ; Ikeda Y ; Matsumoto K ; Ninomiya-Tsuji J Oncogene 2016[Jul]; 35 (29 ): 3829-38 PMID26973245 show ga Sterol-regulatory element-binding proteins (SREBPs) are key transcription factors regulating cholesterol and fatty acid biosynthesis. SREBP activity is tightly regulated to maintain lipid homeostasis, and is modulated upon extracellular stimuli such as growth factors. While the homeostatic SREBP regulation is well studied, stimuli-dependent regulatory mechanisms are still elusive. Here we demonstrate that SREBPs are regulated by a previously uncharacterized mechanism through transforming growth factor-? activated kinase 1 (TAK1), a signaling molecule of inflammation. We found that TAK1 binds to and inhibits mature forms of SREBPs. In an in vivo setting, hepatocyte-specific Tak1 deletion upregulates liver lipid deposition and lipogenic enzymes in the mouse model. Furthermore, hepatic Tak1 deficiency causes steatosis pathologies including elevated blood triglyceride and cholesterol levels, which are established risk factors for the development of hepatocellular carcinoma (HCC) and are indeed correlated with Tak1-deficiency-induced HCC development. Pharmacological inhibition of SREBPs alleviated the steatosis and reduced the expression level of the HCC marker gene in the Tak1-deficient liver. Thus, TAK1 regulation of SREBP critically contributes to the maintenance of liver homeostasis to prevent steatosis, which is a potentially important mechanism to prevent HCC development. |*Homeostasis [MESH] |*Lipid Metabolism [MESH] |Animals [MESH] |Carcinoma, Hepatocellular/genetics/metabolism [MESH] |Cell Line [MESH] |Fatty Liver/genetics/metabolism [MESH] |Female [MESH] |HEK293 Cells [MESH] |Hep G2 Cells [MESH] |Hepatocytes/metabolism [MESH] |Humans [MESH] |Immunoblotting [MESH] |Liver Neoplasms/genetics/metabolism [MESH] |Liver/*metabolism [MESH] |MAP Kinase Kinase Kinases/genetics/*metabolism [MESH] |Male [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Mice, Transgenic [MESH] |Protein Binding [MESH] |RNA Interference [MESH] |Risk Factors [MESH]TAK1 regulates hepatic lipid homeostasis through SREBP (epmc).pdf DeepDyve Pubget Overpricing