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10.1073/pnas.1610617114 http://scihub22266oqcxt.onion/10.1073/pnas.1610617114 C5468679!5468679!28584128     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       Proc+Natl+Acad+Sci+U+S+A 2017 ; 114 (23): 5800-7 Nephropedia Template TP {{tp|p=28584128|t=2017. Bcl11b and combinatorial resolution of cell fate in the T-cell gene regulatory network |pdf=|usr=}}{{28584128}} gab.com Text Bcl11b and combinatorial resolution of cell fate in the T-cell gene regulatory network JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=28584128 #FOAvip T-cell development from hematopoietic progenitors depends on multiple transcription factors, mobilized and modulated by intrathymic Notch signaling. Key aspects of T-cell specification network architecture have been illuminated through recent reports defining roles of transcription factors PU.1, GATA-3, and E2A, their interactions with Notch signaling, and roles of Runx1, TCF-1, and Hes1, providing bases for a comprehensively updated model of the T-cell specification gene regulatory network presented herein. However, the role of lineage commitment factor Bcl11b has been unclear. We use self-organizing maps on 63 RNA-seq datasets from normal and perturbed T-cell development to identify functional targets of Bcl11b during commitment and relate them to other regulomes. We show that both activation and repression target genes can be bound by Bcl11b in vivo, and that Bcl11b effects overlap with E2A-dependent effects. The newly clarified role of Bcl11b distinguishes discrete components of commitment, resolving how innate lymphoid, myeloid, and dendritic, and B-cell fate alternatives are excluded by different mechanisms. Twit Text FOAVip Bcl11b and combinatorial resolution of cell fate in the T-cell gene regulatory network ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=28584128 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28584128 #FOAvip English Wikipedia <ref>{{Cite pmid|28584128}}</ref> Bcl11b and combinatorial resolution of cell fate in the T-cell gene regulatory network #MMPMID28584128 Longabaugh WJR; Zeng W; Zhang JA; Hosokawa H; Jansen CS; Li L; Romero-Wolf M; Liu P; Kueh HY; Mortazavi A; Rothenberg EV Proc Natl Acad Sci U S A 2017[Jun]; 114 (23): 5800-7 PMID28584128show ga T-cell development from hematopoietic progenitors depends on multiple transcription factors, mobilized and modulated by intrathymic Notch signaling. Key aspects of T-cell specification network architecture have been illuminated through recent reports defining roles of transcription factors PU.1, GATA-3, and E2A, their interactions with Notch signaling, and roles of Runx1, TCF-1, and Hes1, providing bases for a comprehensively updated model of the T-cell specification gene regulatory network presented herein. However, the role of lineage commitment factor Bcl11b has been unclear. We use self-organizing maps on 63 RNA-seq datasets from normal and perturbed T-cell development to identify functional targets of Bcl11b during commitment and relate them to other regulomes. We show that both activation and repression target genes can be bound by Bcl11b in vivo, and that Bcl11b effects overlap with E2A-dependent effects. The newly clarified role of Bcl11b distinguishes discrete components of commitment, resolving how innate lymphoid, myeloid, and dendritic, and B-cell fate alternatives are excluded by different mechanisms. äBcl11b and combinatorial resolution of cell fate in the T-cell gene re(epmc).pdf DeepDyve Pubget Overpricing