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10.1016/j.devcel.2012.02.005 http://scihub22266oqcxt.onion/10.1016/j.devcel.2012.02.005 C4047762!4047762!22421041     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       Dev+Cell 2012 ; 22 (3): 489-500 Nephropedia Template TP {{tp|p=22421041|t=2012. ALK1 Signaling Inhibits Angiogenesis by Cooperating with the Notch Pathway |pdf=|usr=}}{{22421041}} gab.com Text ALK1 Signaling Inhibits Angiogenesis by Cooperating with the Notch Pathway JO: Dev Cell http://www.kidney.de/pget.php?&tw=1&pmid=22421041 #FOAvip Activin receptor-like kinase 1 (ALK1) is an endothelial-specific member of the TGF-?/BMP receptor family that is inactivated in patients with hereditary hemorrhagic telangiectasia (HHT). How ALK1 signaling regulates angiogenesis remains incompletely understood. Here we show that ALK1 inhibits angiogenesis by cooperating with the Notch pathway. Blocking Alk1 signaling during postnatal development in mice leads to retinal hypervascularization and the appearance of arteriovenous malformations (AVMs). Combined blockade of Alk1 and Notch signaling further exacerbates hypervascularization, whereas activation of Alk1 by its high-affinity ligand BMP9 rescues hypersprouting induced by Notch inhibition. Mechanistically, ALK1-dependent SMAD signaling synergizes with activated Notch in stalk cells to induce expression of the Notch targets HEY1 and HEY2, thereby repressing VEGF signaling, tip cell formation, and endothelial sprouting. Taken together, these results uncover a direct link between ALK1 and Notch signaling during vascular morpho-genesis that may be relevant to the pathogenesis of HHT vascular lesions. Twit Text FOAVip ALK1 Signaling Inhibits Angiogenesis by Cooperating with the Notch Pathway ????Dev Cell http://www.kidney.de/pget.php?&tw=1&pmid=22421041 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22421041 #FOAvip English Wikipedia <ref>{{Cite pmid|22421041}}</ref> ALK1 Signaling Inhibits Angiogenesis by Cooperating with the Notch Pathway #MMPMID22421041 Larrivée B; Prahst C; Gordon E; del Toro R; Mathivet T; Duarte A; Simons M; Eichmann A Dev Cell 2012[Mar]; 22 (3): 489-500 PMID22421041show ga Activin receptor-like kinase 1 (ALK1) is an endothelial-specific member of the TGF-?/BMP receptor family that is inactivated in patients with hereditary hemorrhagic telangiectasia (HHT). How ALK1 signaling regulates angiogenesis remains incompletely understood. Here we show that ALK1 inhibits angiogenesis by cooperating with the Notch pathway. Blocking Alk1 signaling during postnatal development in mice leads to retinal hypervascularization and the appearance of arteriovenous malformations (AVMs). Combined blockade of Alk1 and Notch signaling further exacerbates hypervascularization, whereas activation of Alk1 by its high-affinity ligand BMP9 rescues hypersprouting induced by Notch inhibition. Mechanistically, ALK1-dependent SMAD signaling synergizes with activated Notch in stalk cells to induce expression of the Notch targets HEY1 and HEY2, thereby repressing VEGF signaling, tip cell formation, and endothelial sprouting. Taken together, these results uncover a direct link between ALK1 and Notch signaling during vascular morpho-genesis that may be relevant to the pathogenesis of HHT vascular lesions. äALK1 Signaling Inhibits Angiogenesis by Cooperating with the Notch Pat(epmc).pdf DeepDyve Pubget Overpricing