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10.1038/ncomms9510 http://scihub22266oqcxt.onion/10.1038/ncomms9510 C4634136!4634136!26465397     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       Nat+Commun 2015 ; 6 (ä): ä Nephropedia Template TP {{tp|p=26465397|t=2015. Notch signal strength controls cell fate in the haemogenic endothelium |pdf=|usr=}}{{26465397}} gab.com Text Notch signal strength controls cell fate in the haemogenic endothelium JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26465397 #FOAvip Acquisition of the arterial and haemogenic endothelium fates concurrently occur in the aorta?gonad?mesonephros (AGM) region prior to haematopoietic stem cell (HSC) generation. The arterial programme depends on Dll4 and the haemogenic endothelium/HSC on Jag1-mediated Notch1 signalling. How Notch1 distinguishes and executes these different programmes in response to particular ligands is poorly understood. By using two Notch1 activation trap mouse models with different sensitivity, here we show that arterial endothelial cells and HSCs originate from distinct precursors, characterized by different Notch1 signal strengths. Microarray analysis on AGM subpopulations demonstrates that the Jag1 ligand stimulates low Notch strength, inhibits the endothelial programme and is permissive for HSC specification. In the absence of Jag1, endothelial cells experience high Dll4-induced Notch activity and select the endothelial programme, thus precluding HSC formation. Interference with the Dll4 signal by ligand-specific blocking antibodies is sufficient to inhibit the endothelial programme and favour specification of the haematopoietic lineage. Twit Text FOAVip Notch signal strength controls cell fate in the haemogenic endothelium ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26465397 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26465397 #FOAvip English Wikipedia <ref>{{Cite pmid|26465397}}</ref> Notch signal strength controls cell fate in the haemogenic endothelium #MMPMID26465397 Gama-Norton L; Ferrando E; Ruiz-Herguido C; Liu Z; Guiu J; Islam ABMMK; Lee SU; Yan M; Guidos CJ; López-Bigas N; Maeda T; Espinosa L; Kopan R; Bigas A Nat Commun 2015[]; 6 (ä): ä PMID26465397show ga Acquisition of the arterial and haemogenic endothelium fates concurrently occur in the aorta?gonad?mesonephros (AGM) region prior to haematopoietic stem cell (HSC) generation. The arterial programme depends on Dll4 and the haemogenic endothelium/HSC on Jag1-mediated Notch1 signalling. How Notch1 distinguishes and executes these different programmes in response to particular ligands is poorly understood. By using two Notch1 activation trap mouse models with different sensitivity, here we show that arterial endothelial cells and HSCs originate from distinct precursors, characterized by different Notch1 signal strengths. Microarray analysis on AGM subpopulations demonstrates that the Jag1 ligand stimulates low Notch strength, inhibits the endothelial programme and is permissive for HSC specification. In the absence of Jag1, endothelial cells experience high Dll4-induced Notch activity and select the endothelial programme, thus precluding HSC formation. Interference with the Dll4 signal by ligand-specific blocking antibodies is sufficient to inhibit the endothelial programme and favour specification of the haematopoietic lineage. äNotch signal strength controls cell fate in the haemogenic endothelium(epmc).pdf DeepDyve Pubget Overpricing