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10.1080/15548627.2017.1307488 http://scihub22266oqcxt.onion/10.1080/15548627.2017.1307488 C5486369!5486369!28350524     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Autophagy 2017 ; 13 (6): 1088-9 Nephropedia Template TP {{tp|p=28350524|t=2017. An ATF4-ATG5 signaling in hypothalamic POMC neurons regulates obesity |pdf=|usr=}}{{28350524}} gab.com Text An ATF4-ATG5 signaling in hypothalamic POMC neurons regulates obesity JO: Autophagy http://www.kidney.de/pget.php?&tw=1&pmid=28350524 #FOAvip ATF4 (activating transcription factor 4) is an important transcription factor that has many biological functions, while its role in hypothalamic POMC (pro-opiomelanocortin-?) neurons in the regulation of energy homeostasis has not been explored. We recently discovered that mice with an Atf4 deletion specific to POMC neurons (PAKO mice) are lean and have higher energy expenditure. Furthermore, these mice are resistant to high-fat diet (HFD)-induced obesity and obesity-related metabolic disorders. Mechanistically, we found the expression of ATG5 (autophagy-related 5) is upregulated in POMC neurons of PAKO mice, and ATF4 regulates ATG5 expression by binding directly to its promoter. Mice with Atf4 and Atg5 double knockout in POMC neurons have reduced energy expenditure and gain more fat mass compared with PAKO mice under a HFD. Finally, the effect of Atf4 knockout in POMC neurons is possibly mediated by enhanced ATG5-dependent macroautophagy/autophagy and ?-melanocyte-stimulating hormone (?-MSH) production in the hypothalamus. Together, this work not only identifies a beneficial role for ATF4 in hypothalamic POMC neurons in the regulation of obesity, but also provides a new potential therapeutic target for obesity and obesity-related metabolic diseases. Twit Text FOAVip An ATF4-ATG5 signaling in hypothalamic POMC neurons regulates obesity ????Autophagy http://www.kidney.de/pget.php?&tw=1&pmid=28350524 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28350524 #FOAvip English Wikipedia <ref>{{Cite pmid|28350524}}</ref> An ATF4-ATG5 signaling in hypothalamic POMC neurons regulates obesity #MMPMID28350524 Xiao Y; Deng Y; Yuan F; Xia T; Liu H; Li Z; Chen S; Liu Z; Ying H; Liu Y; Zhai Q; Guo F Autophagy 2017[]; 13 (6): 1088-9 PMID28350524show ga ATF4 (activating transcription factor 4) is an important transcription factor that has many biological functions, while its role in hypothalamic POMC (pro-opiomelanocortin-?) neurons in the regulation of energy homeostasis has not been explored. We recently discovered that mice with an Atf4 deletion specific to POMC neurons (PAKO mice) are lean and have higher energy expenditure. Furthermore, these mice are resistant to high-fat diet (HFD)-induced obesity and obesity-related metabolic disorders. Mechanistically, we found the expression of ATG5 (autophagy-related 5) is upregulated in POMC neurons of PAKO mice, and ATF4 regulates ATG5 expression by binding directly to its promoter. Mice with Atf4 and Atg5 double knockout in POMC neurons have reduced energy expenditure and gain more fat mass compared with PAKO mice under a HFD. Finally, the effect of Atf4 knockout in POMC neurons is possibly mediated by enhanced ATG5-dependent macroautophagy/autophagy and ?-melanocyte-stimulating hormone (?-MSH) production in the hypothalamus. Together, this work not only identifies a beneficial role for ATF4 in hypothalamic POMC neurons in the regulation of obesity, but also provides a new potential therapeutic target for obesity and obesity-related metabolic diseases. äAn ATF4-ATG5 signaling in hypothalamic POMC neurons regulates obesity (epmc).pdf DeepDyve Pubget Overpricing