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- W2131284305 abstract "The assembly of individual endothelial cells into multicellular tubes is a complex morphogenetic event in vascular development. Extracellular matrix cues and cell–cell junctional communication are fundamental to tube formation. Together they determine the shape of endothelial cells and the tubular structures that they ultimately form. Little is known regarding how mechanical signals are transmitted between cells to control cell shape changes during morphogenesis. Here we provide evidence that the scaffold protein amotL2 is needed for aortic vessel lumen expansion. Using gene inactivation strategies in zebrafish, mouse and endothelial cell culture systems, we show that amotL2 associates to the VE-cadherin adhesion complex where it couples adherens junctions to contractile actin fibres. Inactivation of amotL2 dissociates VE-cadherin from cytoskeletal tensile forces that affect endothelial cell shape. We propose that the VE-cadherin/amotL2 complex is responsible for transmitting mechanical force between endothelial cells for the coordination of cellular morphogenesis consistent with aortic lumen expansion and function. Cell–cell adhesion molecules and the cytoskeleton determine endothelial cell shape during the formation of blood vessels. Here the authors show that the scaffold protein, amotL2, couples adherens junctions to contractile cytoskeletal proteins to coordinate cellular morphogenesis with aortic lumen expansion." @default.
- W2131284305 created "2016-06-24" @default.
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- W2131284305 date "2014-05-07" @default.
- W2131284305 modified "2023-10-18" @default.
- W2131284305 title "AmotL2 links VE-cadherin to contractile actin fibres necessary for aortic lumen expansion" @default.
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- W2131284305 doi "https://doi.org/10.1038/ncomms4743" @default.
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