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10.1038/nature13961 http://scihub22266oqcxt.onion/10.1038/nature13961 C4267857!4267857!25383539     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nature 2014 ; 516 (7529): 112-5 Nephropedia Template TP {{tp|p=25383539|t=2014. Nutrient Sensing Nuclear Receptors Coordinate Autophagy |pdf=|usr=}}{{25383539}} gab.com Text Nutrient Sensing Nuclear Receptors Coordinate Autophagy JO: Nature http://www.kidney.de/pget.php?&tw=1&pmid=25383539 #FOAvip Autophagy is an evolutionally conserved catabolic process that recycles nutrients upon starvation and maintains cellular energy homeostasis1?3. Its acute regulation by nutrient sensing signaling pathways is well described, but its longer-term transcriptional regulation is not. The nuclear receptors PPAR? and FXR are activated in the fasted or fed liver, respectively4,5. Here we show that both regulate hepatic autophagy. Pharmacologic activation of PPAR? reverses the normal suppression of autophagy in the fed state, inducing autophagic lipid degradation, or lipophagy. This response is lost in PPAR? knockout (PPAR??/?) mice, which are partially defective in the induction of autophagy by fasting. Pharmacologic activation of the bile acid receptor FXR strongly suppresses the induction of autophagy in the fasting state, and this response is absent in FXR knockout (FXR?/?) mice, which show a partial defect in suppression of hepatic autophagy in the fed state. PPAR? and FXR compete for binding to shared sites in autophagic gene promoters, with opposite transcriptional outputs. These results reveal complementary, interlocking mechanisms for regulation of autophagy by nutrient status. Twit Text FOAVip Nutrient Sensing Nuclear Receptors Coordinate Autophagy ????Nature http://www.kidney.de/pget.php?&tw=1&pmid=25383539 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25383539 #FOAvip English Wikipedia <ref>{{Cite pmid|25383539}}</ref> Nutrient Sensing Nuclear Receptors Coordinate Autophagy #MMPMID25383539 Lee JM; Wagner M; Xiao R; Kim KH; Feng D; Lazar MA; Moore DD Nature 2014[Dec]; 516 (7529): 112-5 PMID25383539show ga Autophagy is an evolutionally conserved catabolic process that recycles nutrients upon starvation and maintains cellular energy homeostasis1?3. Its acute regulation by nutrient sensing signaling pathways is well described, but its longer-term transcriptional regulation is not. The nuclear receptors PPAR? and FXR are activated in the fasted or fed liver, respectively4,5. Here we show that both regulate hepatic autophagy. Pharmacologic activation of PPAR? reverses the normal suppression of autophagy in the fed state, inducing autophagic lipid degradation, or lipophagy. This response is lost in PPAR? knockout (PPAR??/?) mice, which are partially defective in the induction of autophagy by fasting. Pharmacologic activation of the bile acid receptor FXR strongly suppresses the induction of autophagy in the fasting state, and this response is absent in FXR knockout (FXR?/?) mice, which show a partial defect in suppression of hepatic autophagy in the fed state. PPAR? and FXR compete for binding to shared sites in autophagic gene promoters, with opposite transcriptional outputs. These results reveal complementary, interlocking mechanisms for regulation of autophagy by nutrient status. äNutrient Sensing Nuclear Receptors Coordinate Autophagy (epmc).pdf DeepDyve Pubget Overpricing