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10.2337/db15-1331 http://scihub22266oqcxt.onion/10.2337/db15-1331 C4839200!4839200!26936960     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Diabetes 2016 ; 65 (5): 1208-18 Nephropedia Template TP {{tp|p=26936960|t=2016. Inhibition of TGF-? Signaling Promotes Human Pancreatic ?-Cell Replication |pdf=|usr=}}{{26936960}} gab.com Text Inhibition of TGF- Signaling Promotes Human Pancreatic -Cell Replication JO: Diabetes http://www.kidney.de/pget.php?&tw=1&pmid=26936960 #FOAvip Diabetes is associated with loss of functional pancreatic ?-cells, and restoration of ?-cells is a major goal for regenerative therapies. Endogenous regeneration of ?-cells via ?-cell replication has the potential to restore cellular mass; however, pharmacological agents that promote regeneration or expansion of endogenous ?-cells have been elusive. The regenerative capacity of ?-cells declines rapidly with age, due to accumulation of p16INK4a, resulting in limited capacity for adult endocrine pancreas regeneration. Here, we show that transforming growth factor-? (TGF-?) signaling via Smad3 integrates with the trithorax complex to activate and maintain Ink4a expression to prevent ?-cell replication. Importantly, inhibition of TGF-? signaling can result in repression of the Ink4a/Arf locus, resulting in increased ?-cell replication in adult mice. Furthermore, small molecule inhibitors of the TGF-? pathway promote ?-cell replication in human islets transplanted into NOD-scid IL-2Rgnull mice. These data reveal a novel role for TGF-? signaling in the regulation of the Ink4a/Arf locus and highlight the potential of using small molecule inhibitors of TGF-? signaling to promote human ?-cell replication. Twit Text FOAVip Inhibition of TGF- Signaling Promotes Human Pancreatic -Cell Replication ????Diabetes http://www.kidney.de/pget.php?&tw=1&pmid=26936960 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26936960 #FOAvip English Wikipedia <ref>{{Cite pmid|26936960}}</ref> Inhibition of TGF-? Signaling Promotes Human Pancreatic ?-Cell Replication #MMPMID26936960 Dhawan S; Dirice E; Kulkarni RN; Bhushan A Diabetes 2016[May]; 65 (5): 1208-18 PMID26936960show ga Diabetes is associated with loss of functional pancreatic ?-cells, and restoration of ?-cells is a major goal for regenerative therapies. Endogenous regeneration of ?-cells via ?-cell replication has the potential to restore cellular mass; however, pharmacological agents that promote regeneration or expansion of endogenous ?-cells have been elusive. The regenerative capacity of ?-cells declines rapidly with age, due to accumulation of p16INK4a, resulting in limited capacity for adult endocrine pancreas regeneration. Here, we show that transforming growth factor-? (TGF-?) signaling via Smad3 integrates with the trithorax complex to activate and maintain Ink4a expression to prevent ?-cell replication. Importantly, inhibition of TGF-? signaling can result in repression of the Ink4a/Arf locus, resulting in increased ?-cell replication in adult mice. Furthermore, small molecule inhibitors of the TGF-? pathway promote ?-cell replication in human islets transplanted into NOD-scid IL-2Rgnull mice. These data reveal a novel role for TGF-? signaling in the regulation of the Ink4a/Arf locus and highlight the potential of using small molecule inhibitors of TGF-? signaling to promote human ?-cell replication. äInhibition of TGF-? Signaling Promotes Human Pancreatic ?-Cell Replica(epmc).pdf DeepDyve Pubget Overpricing