ArticleThe EMBO journal2002
VE-PTP and VE-cadherin ectodomains interact to facilitate regulation of phosphorylation and cell contacts.
Article in The EMBO journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 148 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
148 citing papers in PubMed, 1 synthesis or guideline pooled it, 314 citations in OpenAlex.
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- Angiogenesis: Biological Mechanisms and In Vitro Models.Annals of biomedical engineering · 2025Review
- Vascular endothelial growth factor signaling in health and disease: from molecular mechanisms to therapeutic perspectives.Signal transduction and targeted therapy · 2025Review
- New mechanisms and therapeutic approaches to regulate vascular permeability in systemic inflammation.Current opinion in hematology · 2025Review
- Razuprotafib Does Not Improve Microcirculatory Perfusion Disturbances nor Renal Edema in Rats on Extracorporeal Circulation.International journal of molecular sciences · 2025Article
- Plakoglobin does not participate in endothelial barrier stabilization mediated by cAMP.Scientific reports · 2025Article
- Article
- VE-PTP controls a fluid shear stress set point that governs cell morphological responses through Tie-2.Frontiers in cell and developmental biology · 2025Article
- Coagulation factor XI regulates endothelial cell permeability and barrier function in vitro and in vivo.Blood · 2024Article
- VEPTP inhibition with an extracellular domain targeting antibody did not restore albuminuria in a mouse model of diabetic kidney disease.Physiological reports · 2024Article
- Molecular Mechanisms Regulating Vascular Endothelial Permeability.International journal of molecular sciences · 2024Review
- Beyond VEGF: Angiopoietin-Tie Signaling Pathway in Diabetic Retinopathy.Journal of clinical medicine · 2024Review
- trans-Endothelial neutrophil migration activates bactericidal function via Piezo1 mechanosensing.Immunity · 2024Article
- Analysis of Receptor-Type Protein Tyrosine Phosphatase Extracellular Regions with Insights from AlphaFold.International journal of molecular sciences · 2024Review
- Heterogeneity of endothelial VE-PTP downstream polarization, Tie2 activation, junctional claudin-5, and permeability in the aorta and vena cava.Cell and tissue research · 2024Article
- Endothelial barrier dysfunction in systemic inflammation is mediated by soluble VE-cadherin interfering VE-PTP signaling.iScience · 2023Article
- Review
- Shear stress control of vascular leaks and atheromas through Tie2 activation by VE-PTP sequestration.EMBO molecular medicine · 2023Article
- An agonistic anti-Tie2 antibody suppresses the normal-to-tumor vascular transition in the glioblastoma invasion zone.Experimental & molecular medicine · 2023Article
88 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
VE-cadherin is the essential adhesion molecule in endothelial adherens junctions, and the regulation of protein tyrosine phosphorylation is thought to be important for the control of adherens junction integrity. We show here that VE-PTP (vascular endothelial protein tyrosine phosphatase), an endothelial receptor-type phosphatase, co-precipitates with VE-cadherin, but not with beta-catenin, from cell lysates of transfected COS-7 cells and of endothelial cells. Co-precipitation of VE-cadherin and VE-PTP required the most membrane-proximal extracellular domains of each protein. Expression of VE-PTP in triple-transfected COS-7 cells and in CHO cells reversed the tyrosine phosphorylation of VE-cadherin elicited by vascular endothelial growth factor receptor 2 (VEGFR-2). Expression of VE-PTP under an inducible promotor in CHO cells transfected with VE-cadherin and VEGFR-2 increased the VE-cadherin-mediated barrier integrity of a cellular monolayer. Surprisingly, a catalytically inactive mutant form of VE-PTP had the same effect on VE-cadherin phosphorylation and cell layer permeability. Thus, VE-PTP is a transmembrane binding partner of VE-cadherin that associates through an extracellular domain and reduces the tyrosine phosphorylation of VE-cadherin and cell layer permeability independently of its enzymatic activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.