ArticleSmall GTPases2016
Small Rho GTPase-mediated actin dynamics at endothelial adherens junctions.
Article in Small GTPases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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
28 citing papers in PubMed, 54 citations in OpenAlex.
- Piezo1-Src signaling rapidly disrupts brain endothelial barrier integrity.Fluids and barriers of the CNS · 2026Article
- NCKAP1 coordinates focal adhesion and adherens junction dynamics in endothelial barrier maintenance and angiogenesis.iScience · 2026Article
- CSF Leukocytes in Intracranial Infections: Diagnostic, Mechanistic, and Therapeutic Insights for Neurocritical Care.Cellular and molecular neurobiology · 2026Review
- The role of aging on endothelial cell-cell junctions and pulmonary microvascular permeability in male mice.Physiological reports · 2025Article
- Analysis of Vascular Permeability by a Modified Miles Assay.Bio-protocol · 2025Article
- Inhibition of RhoA Prevents Cryptococcus neoformans Capsule Glucuronoxylomannan-Stimulated Brain Endothelial Barrier Disruption.The Journal of infectious diseases · 2024Article
- Off-targets of BRAF inhibitors disrupt endothelial signaling and vascular barrier function.Life science alliance · 2024Article
- Molecular Mechanisms Regulating Vascular Endothelial Permeability.International journal of molecular sciences · 2024Review
- Tankyrase inhibition interferes with junction remodeling, induces leakiness, and disturbs YAP1/TAZ signaling in the endothelium.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- TIMP2 ameliorates blood-brain barrier disruption in traumatic brain injury by inhibiting Src-dependent VE-cadherin internalization.The Journal of clinical investigation · 2023Article
- Lipocalin 10 is essential for protection against inflammation-triggered vascular leakage by activating LDL receptor-related protein 2-slingshot homologue 1 signalling pathway.Cardiovascular research · 2023Article
- Cellular crosstalk in atherosclerotic plaque microenvironment.Cell communication and signaling : CCS · 2023Review
- Review
- KRIT1: A Traffic Warden at the Busy Crossroads Between Redox Signaling and the Pathogenesis of Cerebral Cavernous Malformation Disease.Antioxidants & redox signaling · 2023Review
- Extracellular matrix regulates force transduction at VE-cadherin junctions.Molecular biology of the cell · 2022Article
- Respiratory syncytial virus disrupts the airway epithelial barrier by decreasing cortactin and destabilizing F-actin.Journal of cell science · 2022Article
- Longitudinal genomic alternations and clonal dynamics analysis of primary malignant melanoma of the esophagus.Neoplasia (New York, N.Y.) · 2022Article
- In vivo dissection of Rhoa function in vascular development using zebrafish.Angiogenesis · 2022Article
- Mechanisms Governing Anaphylaxis: Inflammatory Cells, Mediators, Endothelial Gap Junctions and Beyond.International journal of molecular sciences · 2021Review
- Sodium Glucose Co-Transporter 2 Inhibitors Ameliorate Endothelium Barrier Dysfunction Induced by Cyclic Stretch through Inhibition of Reactive Oxygen Species.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
VE-cadherin-based cell-cell junctions form the major restrictive barrier of the endothelium to plasma proteins and blood cells. The function of VE-cadherin and the actin cytoskeleton are intimately linked. Vascular permeability factors and adherent leukocytes signal through small Rho GTPases to tightly regulate actin cytoskeletal rearrangements in order to open and re-assemble endothelial cell-cell junctions in a rapid and controlled manner. The Rho GTPases are activated by guanine nucleotide exchange factors (GEFs), conferring specificity and context-dependent control of cell-cell junctions. Although the molecular mechanisms that couple cadherins to actin filaments are beginning to be elucidated, specific stimulus-dependent regulation of the actin cytoskeleton at VE-cadherin-based junctions remains unexplained. Accumulating evidence has suggested that depending on the vascular permeability factor and on the subcellular localization of GEFs, cell-cell junction dynamics and organization are differentially regulated by one specific Rho GTPase. In this Commentary, we focus on new insights how the junctional actin cytoskeleton is specifically and locally regulated by Rho GTPases and GEFs in the endothelium.
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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.