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10.1242/dev.130575 http://scihub22266oqcxt.onion/10.1242/dev.130575 C4813288!4813288!26893350     free     free     free Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Development 2016 ; 143 (6): 1041-54 Nephropedia Template TP {{tp|p=26893350|t=2016. Wnt/?-catenin signaling enables developmental transitions during valvulogenesis |pdf=|usr=}}{{26893350}} gab.com Text Wnt/ -catenin signaling enables developmental transitions during valvulogenesis JO: Development http://www.kidney.de/pget.php?&tw=1&pmid=26893350 #FOAvip Heart valve development proceeds through coordinated steps by which endocardial cushions (ECs) form thin, elongated and stratified valves. Wnt signaling and its canonical effector ?-catenin are proposed to contribute to endocardial-to-mesenchymal transformation (EMT) through postnatal steps of valvulogenesis. However, genetic redundancy and lethality have made it challenging to define specific roles of the canonical Wnt pathway at different stages of valve formation. We developed a transgenic mouse system that provides spatiotemporal inhibition of Wnt/?-catenin signaling by chemically inducible overexpression of Dkk1. Unexpectedly, this approach indicates canonical Wnt signaling is required for EMT in the proximal outflow tract (pOFT) but not atrioventricular canal (AVC) cushions. Furthermore, Wnt indirectly promotes pOFT EMT through its earlier activity in neighboring myocardial cells or their progenitors. Subsequently, Wnt/?-catenin signaling is activated in cushion mesenchymal cells where it supports FGF-driven expansion of ECs and then AVC valve extracellular matrix patterning. Mice lacking Axin2, a negative Wnt regulator, have larger valves, suggesting that accumulating Axin2 in maturing valves represents negative feedback that restrains tissue overgrowth rather than simply reporting Wnt activity. Disruption of these Wnt/?-catenin signaling roles that enable developmental transitions during valvulogenesis could account for common congenital valve defects. Twit Text FOAVip Wnt/ -catenin signaling enables developmental transitions during valvulogenesis ????Development http://www.kidney.de/pget.php?&tw=1&pmid=26893350 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26893350 #FOAvip English Wikipedia <ref>{{Cite pmid|26893350}}</ref> Wnt/?-catenin signaling enables developmental transitions during valvulogenesis #MMPMID26893350 Bosada FM; Devasthali V; Jones KA; Stankunas K Development 2016[Mar]; 143 (6): 1041-54 PMID26893350show ga Heart valve development proceeds through coordinated steps by which endocardial cushions (ECs) form thin, elongated and stratified valves. Wnt signaling and its canonical effector ?-catenin are proposed to contribute to endocardial-to-mesenchymal transformation (EMT) through postnatal steps of valvulogenesis. However, genetic redundancy and lethality have made it challenging to define specific roles of the canonical Wnt pathway at different stages of valve formation. We developed a transgenic mouse system that provides spatiotemporal inhibition of Wnt/?-catenin signaling by chemically inducible overexpression of Dkk1. Unexpectedly, this approach indicates canonical Wnt signaling is required for EMT in the proximal outflow tract (pOFT) but not atrioventricular canal (AVC) cushions. Furthermore, Wnt indirectly promotes pOFT EMT through its earlier activity in neighboring myocardial cells or their progenitors. Subsequently, Wnt/?-catenin signaling is activated in cushion mesenchymal cells where it supports FGF-driven expansion of ECs and then AVC valve extracellular matrix patterning. Mice lacking Axin2, a negative Wnt regulator, have larger valves, suggesting that accumulating Axin2 in maturing valves represents negative feedback that restrains tissue overgrowth rather than simply reporting Wnt activity. Disruption of these Wnt/?-catenin signaling roles that enable developmental transitions during valvulogenesis could account for common congenital valve defects. äWnt/?-catenin signaling enables developmental transitions during valvu(epmc).pdf DeepDyve Pubget Overpricing