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Experimental Cell Research
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publication venue for: VE-cadherin increases the half-life of VEGF receptor 2
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Juvenile Diabetes Research Foundation United States of America, JDRF
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funding vehicle for: VE-cadherin increases the half-life of VEGF receptor 2

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RDF description of VE-cadherin increases the half-life of VEGF receptor 2 - http://orbis.uaslp.mx/vivo/individual/scopus1290
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date: 2026-08-27T20:17:14
publisher: vivo
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Article
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VE-cadherin increases the half-life of VEGF receptor 2
type: Document
page start: 248
freetext keyword: aortic endothelial cells; protein half-life; VE-cadherin; VEGF signaling; VEGFR-2 cadherin; mitogen activated protein kinase; nerve cell adhesion molecule; unclassified drug; uvomorulin; vascular endothelial cadherin; vasculotropin receptor 2; animal cell; article; cattle; controlled study; endothelium cell; half life time; nonhuman; priority journal; protein domain; protein expression; signal transduction
has funding vehicle: Juvenile Diabetes Research Foundation United States of America, JDRF
crisid: 1291
type: Generically Dependent Continuant
type: Continuant
chemicalscas: mitogen activated protein kinase, 142243-02-5; uvomorulin, 112956-45-3
date time value: article date 1291
most specific type: Document
related by: authorship 7600
type: Thing
origen: scopus
has publication venue: Experimental Cell Research
type: Information Content Entity
volume: 300
page end: 256
related by: authorship 7599
most specific type: Article
type: Entity
type: Article
related by: authorship 7598
doi: 10.1016/j.yexcr.2004.07.007
e iscopus: 2-s2.0-4644224489
issue: 1
abstract: VE-cadherin plays a critical role in cell-cell interactions by forming adherens junctions in endothelial cells. VE-cadherin has increasingly been implicated in the cell signaling cascades initiated by the activation of growth factor receptors. Vascular endothelial growth factor receptor 2 (VEGFR-2) is present in regions of cell-cell contact and coimmunoprecipitates with VE-cadherin. In this study, we report that stable overexpression of VE-cadherin in two different endothelial cells induced an increase in VEGFR-2 protein levels. The increase in VEGFR-2 was also induced by overexpression of other classical cadherins such as E-cadherin or N-cadherin. Removing the extracellular domain of VE-cadherin abolished this effect, and a truncated form of VE-cadherin lacking the intracellular domain decreased VEGFR-2 instead of increasing it. VE-cadherin-induced changes in VEGFR-2 levels were paralleled by a corresponding shift in the VEGF-dependent activation of MAPK signaling, which demonstrated the functional relevance of varying the VEGFR-2 levels. Since VE-cadherin upregulated endogenous VEGFR-2 or exogenously expressed VEGFR-2, we hypothesized that the mechanism may be posttranslational. Indeed, the half-life of VEGFR-2 was 70 min in control cells whereas in cells overexpressing VE-cadherin the half-life was extended to 146 min. These results support the existence of a novel layer of functional regulation of VEGFR-2 by VE-cadherin. © 2004 Elsevier Inc. All rights reserved.
estado: published