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10.1016/j.molcel.2014.07.011 http://scihub22266oqcxt.onion/10.1016/j.molcel.2014.07.011 C4228935!4228935!25155613     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25155613&cmd=llinks): Failed to open stream: HTTP request failed! 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SIRT1-mediated deacetylation of CRABPII regulates cellular retinoic acid signaling and modulates embryonic stem cell differentiation |pdf=|usr=}}{{25155613}} gab.com Text SIRT1-mediated deacetylation of CRABPII regulates cellular retinoic acid signaling and modulates embryonic stem cell differentiation JO: Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=25155613 #FOAvip Retinoid homeostasis is critical for normal embryonic development. Both the deficiency and excess of these compounds are associated with congenital malformations. Here we demonstrate that SIRT1, the most conserved mammalian NAD+-dependent protein deacetylase, contributes to homeostatic retinoic acid (RA) signaling and modulates mouse embryonic stem cell (mESC) differentiation in part through deacetylation of cellular retinoic acid binding protein II (CRABPII). We show that RA-mediated acetylation of CRABPII at K102 is essential for its nuclear accumulation and subsequent activation of RA signaling. SIRT1 interacts with and deacetylates CRABPII, regulating its subcellular localization. Consequently, SIRT1 deficiency induces hyper-acetylation and nuclear accumulation of CRABPII, enhancing RA signaling and accelerating mESC differentiation in response to RA. Consistently, SIRT1 deficiency is associated with elevated RA signaling and development defects in mice. Our findings reveal a novel molecular mechanism that regulates RA signaling, and highlight the importance of SIRT1 in regulation of ESC pluripotency and embryogenesis. Twit Text FOAVip SIRT1-mediated deacetylation of CRABPII regulates cellular retinoic acid signaling and modulates embryonic stem cell differentiation ????Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=25155613 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25155613 #FOAvip English Wikipedia <ref>{{Cite pmid|25155613}}</ref> SIRT1-mediated deacetylation of CRABPII regulates cellular retinoic acid signaling and modulates embryonic stem cell differentiation #MMPMID25155613 Tang S; Huang G; Fan W; Chen Y; Ward JM; Xu X; Xu Q; Kang A; McBurney MW; Fargo DC; Hu G; Baumgart-Vogt E; Zhao Y; Li X Mol Cell 2014[Sep]; 55 (6): 843-55 PMID25155613show ga Retinoid homeostasis is critical for normal embryonic development. Both the deficiency and excess of these compounds are associated with congenital malformations. Here we demonstrate that SIRT1, the most conserved mammalian NAD+-dependent protein deacetylase, contributes to homeostatic retinoic acid (RA) signaling and modulates mouse embryonic stem cell (mESC) differentiation in part through deacetylation of cellular retinoic acid binding protein II (CRABPII). We show that RA-mediated acetylation of CRABPII at K102 is essential for its nuclear accumulation and subsequent activation of RA signaling. SIRT1 interacts with and deacetylates CRABPII, regulating its subcellular localization. Consequently, SIRT1 deficiency induces hyper-acetylation and nuclear accumulation of CRABPII, enhancing RA signaling and accelerating mESC differentiation in response to RA. Consistently, SIRT1 deficiency is associated with elevated RA signaling and development defects in mice. Our findings reveal a novel molecular mechanism that regulates RA signaling, and highlight the importance of SIRT1 in regulation of ESC pluripotency and embryogenesis. äSIRT1-mediated deacetylation of CRABPII regulates cellular retinoic ac(epmc).pdf DeepDyve Pubget Overpricing