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10.1016/j.stem.2016.03.002 http://scihub22266oqcxt.onion/10.1016/j.stem.2016.03.002 C4860147!4860147!27053300     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 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 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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27053300.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cell+Stem+Cell 2016 ; 18 (5): 668-81 Nephropedia Template TP {{tp|p=27053300|t=2016. TGF-? Inhibition Rescues Hematopoietic Stem Cell Defects and Bone Marrow Failure in Fanconi Anemia |pdf=|usr=}}{{27053300}} gab.com Text TGF- Inhibition Rescues Hematopoietic Stem Cell Defects and Bone Marrow Failure in Fanconi Anemia JO: Cell Stem Cell http://www.kidney.de/pget.php?&tw=1&pmid=27053300 #FOAvip Fanconi Anemia (FA) is an inherited DNA repair disorder characterized by progressive bone marrow failure (BMF) from hematopoietic stem and progenitor cell (HSPC) attrition. A greater understanding of the pathogenesis of BMF could improve the therapeutic options for FA patients. Using a genome-wide shRNA screen in human FA fibroblasts, we identify transforming growth factor-? (TGF-?) pathway-mediated growth suppression as a cause of BMF in FA. Blocking the TGF-? pathway improves the survival of FA cells and rescues the proliferative and functional defects of HSPCs derived from FA mice and FA patients. Inhibition of TGF-? signaling in FA HSPCs results in elevated homologous recombination (HR) repair with a concomitant decrease in non-homologous end-joining (NHEJ), accounting for the improvement in cellular growth. Together, our results suggest that elevated TGF-? signaling contributes to the BMF in FA by impairing HSPC function, and may be a potential therapeutic target for the treatment of FA. Twit Text FOAVip TGF- Inhibition Rescues Hematopoietic Stem Cell Defects and Bone Marrow Failure in Fanconi Anemia ????Cell Stem Cell http://www.kidney.de/pget.php?&tw=1&pmid=27053300 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27053300 #FOAvip English Wikipedia <ref>{{Cite pmid|27053300}}</ref> TGF-? Inhibition Rescues Hematopoietic Stem Cell Defects and Bone Marrow Failure in Fanconi Anemia #MMPMID27053300 Zhang H; Kozono DE; O?Connor KW; Vidal-Cardenas S; Rousseau A; Hamilton A; Moreau L; Gaudiano EF; Greenberger J; Bagby G; Soulier J; Grompe M; Parmar K; D?Andrea AD Cell Stem Cell 2016[May]; 18 (5): 668-81 PMID27053300show ga Fanconi Anemia (FA) is an inherited DNA repair disorder characterized by progressive bone marrow failure (BMF) from hematopoietic stem and progenitor cell (HSPC) attrition. A greater understanding of the pathogenesis of BMF could improve the therapeutic options for FA patients. Using a genome-wide shRNA screen in human FA fibroblasts, we identify transforming growth factor-? (TGF-?) pathway-mediated growth suppression as a cause of BMF in FA. Blocking the TGF-? pathway improves the survival of FA cells and rescues the proliferative and functional defects of HSPCs derived from FA mice and FA patients. Inhibition of TGF-? signaling in FA HSPCs results in elevated homologous recombination (HR) repair with a concomitant decrease in non-homologous end-joining (NHEJ), accounting for the improvement in cellular growth. Together, our results suggest that elevated TGF-? signaling contributes to the BMF in FA by impairing HSPC function, and may be a potential therapeutic target for the treatment of FA. äTGF-? Inhibition Rescues Hematopoietic Stem Cell Defects and Bone Marr(epmc).pdf DeepDyve Pubget Overpricing