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10.1242/dev.112532 http://scihub22266oqcxt.onion/10.1242/dev.112532 C4325377!4325377!25617435     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25617435&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Development 2015 ; 142 (4): 774-86 Nephropedia Template TP {{tp|p=25617435|t=2015. UXT potentiates angiogenesis by attenuating Notch signaling |pdf=|usr=}}{{25617435}} gab.com Text UXT potentiates angiogenesis by attenuating Notch signaling JO: Development http://www.kidney.de/pget.php?&tw=1&pmid=25617435 #FOAvip Angiogenesis is spatially and temporally orchestrated by a myriad of signaling pathways, including the Notch signaling pathway. Here, we identified UXT as an evolutionarily conserved and developmentally expressed protein, indispensable for intersegmental vessel (ISV) formation in zebrafish. Deficiency of UXT in zebrafish embryos results in shorter ISVs, loss of tip cell behavior, and impairment of endothelial cell migration and division. Significantly, UXT attenuates the expression of the Notch-responsive genes in vitro and in vivo. Mechanistically, UXT binds to the promoters of the Notch signaling target genes and specifically interacts with the transactivation region domain of the Notch intracellular domain (NICD), impairing the interaction between NICD and the transcription factor RBP-J? endogenously. This prevents RBP-J?/CSL from activation and thus inhibits the consequent gene inductions. Furthermore, blockade of Notch signaling rescues the angiogenesis defect caused by UXT knockdown both in vitro and in vivo. Taken together, the data presented in this study characterize UXT as a novel repressor of Notch signaling, shedding new light on the molecular regulation of angiogenesis. Twit Text FOAVip UXT potentiates angiogenesis by attenuating Notch signaling ????Development http://www.kidney.de/pget.php?&tw=1&pmid=25617435 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25617435 #FOAvip English Wikipedia <ref>{{Cite pmid|25617435}}</ref> UXT potentiates angiogenesis by attenuating Notch signaling #MMPMID25617435 Zhou Y; Ge R; Wang R; Liu F; Huang Y; Liu H; Hao Y; Zhou Q; Wang C Development 2015[Feb]; 142 (4): 774-86 PMID25617435show ga Angiogenesis is spatially and temporally orchestrated by a myriad of signaling pathways, including the Notch signaling pathway. Here, we identified UXT as an evolutionarily conserved and developmentally expressed protein, indispensable for intersegmental vessel (ISV) formation in zebrafish. Deficiency of UXT in zebrafish embryos results in shorter ISVs, loss of tip cell behavior, and impairment of endothelial cell migration and division. Significantly, UXT attenuates the expression of the Notch-responsive genes in vitro and in vivo. Mechanistically, UXT binds to the promoters of the Notch signaling target genes and specifically interacts with the transactivation region domain of the Notch intracellular domain (NICD), impairing the interaction between NICD and the transcription factor RBP-J? endogenously. This prevents RBP-J?/CSL from activation and thus inhibits the consequent gene inductions. Furthermore, blockade of Notch signaling rescues the angiogenesis defect caused by UXT knockdown both in vitro and in vivo. Taken together, the data presented in this study characterize UXT as a novel repressor of Notch signaling, shedding new light on the molecular regulation of angiogenesis. äUXT potentiates angiogenesis by attenuating Notch signaling (epmc).pdf DeepDyve Pubget Overpricing