VEGF controls endothelial-cell permeability by promoting the β-arrestin-dependent endocytosis of VE-cadherin

By J. Gavard, J. Gutkind. Nature Cell Biology, 2006

859 citations recorded by the source corpus.

Subfields: Immunology and Allergy, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/606767932f8bc6b1ed2b869c69ed85ce4027a0a5

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Citations in the corpus

Mechanisms of Leukocyte Transendothelial Migration (2011, background): “In other systems, Rac1 activation leads to phosphorylation of VE-cadherin on serine 665, which signals its clathrin-dependent internalization (65).”
The role of adherens junctions and VE-cadherin in the control of vascular permeability (2008, background): “In a recent report, it was found that VEGF disrupts endothelial-barrier function by activating SRC, which, in turn, phosphorylates VAV2, a guanine-nucleotideexchange factor (GEF) for the GTPase Rac (Gavard and Gutkind, 2006).”
Adherens junctions: from molecules to morphogenesis (2010, background): “For example, the clathrin adaptor β-arrestin interacts with VE-cadherin when it is phosphorylated at its juxtamembrane domain, promoting endocytosi”
The blood-brain barrier in brain homeostasis and neurological diseases. (2009, neutral): “Recent data showed that VEGF, an angiogenic growth factor known to be produced at a high level in brain tumors [147,148], promoted endocytosis of the endothelial cell adhesion molecule VEcadherin, leading to disruption of the endothelial barrier function and increase in endothelial permeability [149”
Neuroinflammatory mechanisms of blood-brain barrier damage in ischemic stroke. (2019, background): “VEGF promotes the internalization of VE-cadherin, which results in endothelial barrier disruption (66, 209).”
Signal transduction by vascular endothelial growth factor receptors. (2012, background): “VEGF may also regulate junctional permeability by stimulating endocytosis of VE-cadherin, by sequential activation of SRC-VAV2-RAC and PAK, followed by serine phosphorylation of VE-cadherin (Fig.”
Derailed endocytosis: an emerging feature of cancer (2008, background): “Endocytosis of a key endothelial cell adhesion molecule, VE-cadherin , is regulated by vascular endothelial growth factor A ( VEGFA ) through a different mechanism: p21-activated kinase (PAK) phosphorylates a highly conserved motif within the intracellular tail of VE-cadherin, which results in the ”
Vascular endothelial growth factor in eye disease. (2008, background): “[PubMed: 15939038] Navaratna D, McGuire PG, et al. Proteolytic degradation of VE-cadherin alters the blood-retinal barrier in diabetes.”