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10.1038/ncomms15652 http://scihub22266oqcxt.onion/10.1038/ncomms15652 C5467166!5467166!28585545     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       Nat+Commun 2017 ; 8 (ä): ä Nephropedia Template TP {{tp|p=28585545|t=2017. Sox5 regulates beta-cell phenotype and is reduced in type 2 diabetes |pdf=|usr=}}{{28585545}} gab.com Text Sox5 regulates beta-cell phenotype and is reduced in type 2 diabetes JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=28585545 #FOAvip Type 2 diabetes (T2D) is characterized by insulin resistance and impaired insulin secretion, but the mechanisms underlying insulin secretion failure are not completely understood. Here, we show that a set of co-expressed genes, which is enriched for genes with islet-selective open chromatin, is associated with T2D. These genes are perturbed in T2D and have a similar expression pattern to that of dedifferentiated islets. We identify Sox5 as a regulator of the module. Sox5 knockdown induces gene expression changes similar to those observed in T2D and diabetic animals and has profound effects on insulin secretion, including reduced depolarization-evoked Ca2+-influx and ?-cell exocytosis. SOX5 overexpression reverses the expression perturbations observed in a mouse model of T2D, increases the expression of key ?-cell genes and improves glucose-stimulated insulin secretion in human islets from donors with T2D. We suggest that human islets in T2D display changes reminiscent of dedifferentiation and highlight SOX5 as a regulator of ?-cell phenotype and function. Twit Text FOAVip Sox5 regulates beta-cell phenotype and is reduced in type 2 diabetes ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=28585545 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28585545 #FOAvip English Wikipedia <ref>{{Cite pmid|28585545}}</ref> Sox5 regulates beta-cell phenotype and is reduced in type 2 diabetes #MMPMID28585545 Axelsson AS; Mahdi T; Nenonen HA; Singh T; Hänzelmann S; Wendt A; Bagge A; Reinbothe TM; Millstein J; Yang X; Zhang B; Gusmao EG; Shu L; Szabat M; Tang Y; Wang J; Salö S; Eliasson L; Artner I; Fex M; Johnson JD; Wollheim CB; Derry J; Mecham B; Spégel P; Mulder H; Costa I; Zhang E; Rosengren AH Nat Commun 2017[]; 8 (ä): ä PMID28585545show ga Type 2 diabetes (T2D) is characterized by insulin resistance and impaired insulin secretion, but the mechanisms underlying insulin secretion failure are not completely understood. Here, we show that a set of co-expressed genes, which is enriched for genes with islet-selective open chromatin, is associated with T2D. These genes are perturbed in T2D and have a similar expression pattern to that of dedifferentiated islets. We identify Sox5 as a regulator of the module. Sox5 knockdown induces gene expression changes similar to those observed in T2D and diabetic animals and has profound effects on insulin secretion, including reduced depolarization-evoked Ca2+-influx and ?-cell exocytosis. SOX5 overexpression reverses the expression perturbations observed in a mouse model of T2D, increases the expression of key ?-cell genes and improves glucose-stimulated insulin secretion in human islets from donors with T2D. We suggest that human islets in T2D display changes reminiscent of dedifferentiation and highlight SOX5 as a regulator of ?-cell phenotype and function. äSox5 regulates beta-cell phenotype and is reduced in type 2 diabetes (epmc).pdf DeepDyve Pubget Overpricing