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10.1038/nature15729 http://scihub22266oqcxt.onion/10.1038/nature15729 C4826614!4826614!26618866     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nature 2015 ; 528 (7583): 510-6 Nephropedia Template TP {{tp|p=26618866|t=2015. ?F508 CFTR interactome remodeling promotes rescue of Cystic Fibrosis |pdf=|usr=}}{{26618866}} gab.com Text F508 CFTR interactome remodeling promotes rescue of Cystic Fibrosis JO: Nature http://www.kidney.de/pget.php?&tw=1&pmid=26618866 #FOAvip Deletion of phenylalanine 508 of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) is the major cause of Cystic Fibrosis (CF), one of the most common inherited childhood diseases. The mutated CFTR anion channel is not fully glycosylated and shows minimal activity in bronchial epithelial cells of CF patients. Low temperature or inhibition of histone deacetylases (HDACi) can partially rescue ?F508 CFTR cellular processing defects and function. A favorable change of ?F508 CFTR protein-protein interactions was proposed as mechanism of rescue, however CFTR interactome dynamics during temperature-shift and HDACi rescue are unknown. Here, we report the first comprehensive analysis of the wt and ?F508 CFTR interactome and its dynamics during temperature shift and HDACi. By using a novel deep proteomic analysis method (CoPIT), we identified 638 individual high-confidence CFTR interactors and discovered a mutation-specific interactome, which is extensively remodeled upon rescue. Detailed analysis of the interactome remodeling identified key novel interactors, whose loss promoted enhanced CFTR channel function in primary CF epithelia or which were critical for normal CFTR biogenesis. Our results demonstrate that global remodeling of ?F508 CFTR interactions is crucial for rescue, and provide comprehensive insight into the molecular disease mechanisms of CF caused by deletion of F508. Twit Text FOAVip F508 CFTR interactome remodeling promotes rescue of Cystic Fibrosis ????Nature http://www.kidney.de/pget.php?&tw=1&pmid=26618866 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26618866 #FOAvip English Wikipedia <ref>{{Cite pmid|26618866}}</ref> ?F508 CFTR interactome remodeling promotes rescue of Cystic Fibrosis #MMPMID26618866 Pankow S; Bamberger C; Calzolari D; Martínez-Bartolomé S; Lavallée-Adam M; Balch WE; Yates JR Nature 2015[Dec]; 528 (7583): 510-6 PMID26618866show ga Deletion of phenylalanine 508 of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) is the major cause of Cystic Fibrosis (CF), one of the most common inherited childhood diseases. The mutated CFTR anion channel is not fully glycosylated and shows minimal activity in bronchial epithelial cells of CF patients. Low temperature or inhibition of histone deacetylases (HDACi) can partially rescue ?F508 CFTR cellular processing defects and function. A favorable change of ?F508 CFTR protein-protein interactions was proposed as mechanism of rescue, however CFTR interactome dynamics during temperature-shift and HDACi rescue are unknown. Here, we report the first comprehensive analysis of the wt and ?F508 CFTR interactome and its dynamics during temperature shift and HDACi. By using a novel deep proteomic analysis method (CoPIT), we identified 638 individual high-confidence CFTR interactors and discovered a mutation-specific interactome, which is extensively remodeled upon rescue. Detailed analysis of the interactome remodeling identified key novel interactors, whose loss promoted enhanced CFTR channel function in primary CF epithelia or which were critical for normal CFTR biogenesis. Our results demonstrate that global remodeling of ?F508 CFTR interactions is crucial for rescue, and provide comprehensive insight into the molecular disease mechanisms of CF caused by deletion of F508. ä?F508 CFTR interactome remodeling promotes rescue of Cystic Fibrosis (epmc).pdf DeepDyve Pubget Overpricing