Evidence map›Paper›PMID 42006337›Full record

ArticleiScience2026

VE-cadherin interaction proteomics identifies ARVCF as stabilizer of endothelial adherens junctions.

Rianne M Schoon, Tsveta S van Krimpen-Malinova, Iris de Heer, Arie J Hoogendijk, Floris P J van Alphen, Annett de Haan, Anne-Marieke D van Stalborch, Simon Tol, Jaap D van Buul, Maartje van den Biggelaar and 1 more

Abstract read
In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Rianne M SchoonAmsterdam UMC, University of Amsterdam, Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, 1105 AZ Amsterdam, the Netherlands.
Tsveta S van Krimpen-MalinovaAmsterdam UMC, University of Amsterdam, Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, 1105 AZ Amsterdam, the Netherlands.
Iris de HeerAmsterdam UMC, University of Amsterdam, Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, 1105 AZ Amsterdam, the Netherlands.
Arie J HoogendijkDepartment of Molecular Hematology, Joint-AMC-Sanquin Landsteiner Laboratory, 1066 CX Amsterdam, the Netherlands.
Floris P J van AlphenDepartment of Molecular Hematology, Joint-AMC-Sanquin Landsteiner Laboratory, 1066 CX Amsterdam, the Netherlands.
Annett de HaanAmsterdam UMC, University of Amsterdam, Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, 1105 AZ Amsterdam, the Netherlands.
Anne-Marieke D van StalborchAmsterdam UMC, University of Amsterdam, Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, 1105 AZ Amsterdam, the Netherlands.
Simon TolDepartment of Molecular Hematology, Joint-AMC-Sanquin Landsteiner Laboratory, 1066 CX Amsterdam, the Netherlands.
Jaap D van BuulAmsterdam UMC, University of Amsterdam, Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, 1105 AZ Amsterdam, the Netherlands.
Maartje van den BiggelaarDepartment of Molecular Hematology, Joint-AMC-Sanquin Landsteiner Laboratory, 1066 CX Amsterdam, the Netherlands.
Stephan HuveneersAmsterdam UMC, University of Amsterdam, Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, 1105 AZ Amsterdam, the Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Blood vessel integrity is maintained by vascular endothelial-cadherin (VE-cadherin)-based adherens junctions, which form structural links between neighboring endothelial cells. In this study, we used mass spectrometry to identify the key proteins that interact with VE-cadherin. The proteomics identified a core group of proteins that bind to VE-cadherin, even when its intracellular domain is not tyrosine phosphorylated. The core VE-cadherin interactome includes known catenin proteins as well as ARVCF, ARHGAP23, KEAP1, and NGLY1. Co-immunoprecipitation and co-localization experiments verified that the VE-cadherin-binding protein ARVCF is a component of endothelial adherens junctions. During junction maturation, ARVCF selectively binds to a pool of VE-cadherin, which is unbound from p120-catenin, through a mechanism involving its C-terminal intrinsically disordered regions. Depletion of ARVCF results in unstable junctions, loss of endothelial barrier function, and impaired collective cell migration. Together, the results of this study demonstrate that ARVCF is an important stabilizer of VE-cadherin junctions to safeguard endothelial integrity.

Indexed as

BiochemistryCell biologyVascular cell adhesion

Identifiers

PMID42006337
PMCPMC13089046

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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.