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10.1016/j.stemcr.2017.07.002 http://scihub22266oqcxt.onion/10.1016/j.stemcr.2017.07.002 C5599184!5599184!28781078     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Stem+Cell+Reports 2017 ; 9 (3): 913-26 Nephropedia Template TP {{tp|p=28781078|t=2017. NAC1 Regulates Somatic Cell Reprogramming by Controlling Zeb1 and E-cadherin Expression |pdf=|usr=}}{{28781078}} gab.com Text NAC1 Regulates Somatic Cell Reprogramming by Controlling Zeb1 and E-cadherin Expression JO: Stem Cell Reports http://www.kidney.de/pget.php?&tw=1&pmid=28781078 #FOAvip Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) is a long and inefficient process. A thorough understanding of the molecular mechanisms underlying reprogramming is paramount for efficient generation and safe application of iPSCs in medicine. While intensive efforts have been devoted to identifying reprogramming facilitators and barriers, a full repertoire of such factors, as well as their mechanistic actions, is poorly defined. Here, we report that NAC1, a pluripotency-associated factor and NANOG partner, is required for establishment of pluripotency during reprogramming. Mechanistically, NAC1 is essential for proper expression of E-cadherin by a dual regulatory mechanism: it facilitates NANOG binding to the E-cadherin promoter and fine-tunes its expression; most importantly, it downregulates the E-cadherin repressor ZEB1 directly via transcriptional repression and indirectly via post-transcriptional activation of the miR-200 miRNAs. Our study thus uncovers a previously unappreciated role for the pluripotency regulator NAC1 in promoting efficient somatic cell reprogramming. Twit Text FOAVip NAC1 Regulates Somatic Cell Reprogramming by Controlling Zeb1 and E-cadherin Expression ????Stem Cell Reports http://www.kidney.de/pget.php?&tw=1&pmid=28781078 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28781078 #FOAvip English Wikipedia <ref>{{Cite pmid|28781078}}</ref> NAC1 Regulates Somatic Cell Reprogramming by Controlling Zeb1 and E-cadherin Expression #MMPMID28781078 Faiola F; Yin N; Fidalgo M; Huang X; Saunders A; Ding J; Guallar D; Dang B; Wang J Stem Cell Reports 2017[Sep]; 9 (3): 913-26 PMID28781078show ga Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) is a long and inefficient process. A thorough understanding of the molecular mechanisms underlying reprogramming is paramount for efficient generation and safe application of iPSCs in medicine. While intensive efforts have been devoted to identifying reprogramming facilitators and barriers, a full repertoire of such factors, as well as their mechanistic actions, is poorly defined. Here, we report that NAC1, a pluripotency-associated factor and NANOG partner, is required for establishment of pluripotency during reprogramming. Mechanistically, NAC1 is essential for proper expression of E-cadherin by a dual regulatory mechanism: it facilitates NANOG binding to the E-cadherin promoter and fine-tunes its expression; most importantly, it downregulates the E-cadherin repressor ZEB1 directly via transcriptional repression and indirectly via post-transcriptional activation of the miR-200 miRNAs. Our study thus uncovers a previously unappreciated role for the pluripotency regulator NAC1 in promoting efficient somatic cell reprogramming. äNAC1 Regulates Somatic Cell Reprogramming by Controlling Zeb1 and E-ca(epmc).pdf DeepDyve Pubget Overpricing