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10.1038/ncomms12652 http://scihub22266oqcxt.onion/10.1038/ncomms12652 C4999520!4999520!27554288     free     free     free Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2016 ; 7 (ä): ä Nephropedia Template TP {{tp|p=27554288|t=2016. The aryl hydrocarbon receptor controls cyclin O to promote epithelial multiciliogenesis |pdf=|usr=}}{{27554288}} gab.com Text The aryl hydrocarbon receptor controls cyclin O to promote epithelial multiciliogenesis JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=27554288 #FOAvip Epithelia function as barriers against environmental insults and express the transcription factor aryl hydrocarbon receptor (AhR). However, AhR function in these tissues is unknown. Here we show that AhR regulates multiciliogenesis in both murine airway epithelia and in Xenopus laevis epidermis. In air-exposed airway epithelia, induction of factors required for multiciliogenesis, including cyclin O (Ccno) and Multicilin (Mcidas), is AhR dependent, and air exposure induces AhR binding to the Ccno promoter. Submersion and hypoxic conditions impede AhR-dependent Ccno induction. This is mediated by the persistence of Notch signalling, as Notch blockade renders multiciliogenesis and Ccno induction by AhR independent from air exposure. In contrast to Ccno induction, air exposure does not induce the canonical AhR target cytochrome P450 1a1 (Cyp1a1). Inversely, exposure to AhR ligands induces Cyp1a1 but not Ccno and impeded ciliogenesis. These data indicate that AhR involvement in detoxification of environmental pollutants may impede its physiological role, resulting in respiratory pathology. Twit Text FOAVip The aryl hydrocarbon receptor controls cyclin O to promote epithelial multiciliogenesis ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=27554288 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27554288 #FOAvip English Wikipedia <ref>{{Cite pmid|27554288}}</ref> The aryl hydrocarbon receptor controls cyclin O to promote epithelial multiciliogenesis #MMPMID27554288 Villa M; Crotta S; Dingwell KS; Hirst EMA; Gialitakis M; Ahlfors H; Smith JC; Stockinger B; Wack A Nat Commun 2016[]; 7 (ä): ä PMID27554288show ga Epithelia function as barriers against environmental insults and express the transcription factor aryl hydrocarbon receptor (AhR). However, AhR function in these tissues is unknown. Here we show that AhR regulates multiciliogenesis in both murine airway epithelia and in Xenopus laevis epidermis. In air-exposed airway epithelia, induction of factors required for multiciliogenesis, including cyclin O (Ccno) and Multicilin (Mcidas), is AhR dependent, and air exposure induces AhR binding to the Ccno promoter. Submersion and hypoxic conditions impede AhR-dependent Ccno induction. This is mediated by the persistence of Notch signalling, as Notch blockade renders multiciliogenesis and Ccno induction by AhR independent from air exposure. In contrast to Ccno induction, air exposure does not induce the canonical AhR target cytochrome P450 1a1 (Cyp1a1). Inversely, exposure to AhR ligands induces Cyp1a1 but not Ccno and impeded ciliogenesis. These data indicate that AhR involvement in detoxification of environmental pollutants may impede its physiological role, resulting in respiratory pathology. äThe aryl hydrocarbon receptor controls cyclin O to promote epithelial (epmc).pdf DeepDyve Pubget Overpricing