ArticleJournal of cellular physiology2011
R-Ras interacts with filamin a to maintain endothelial barrier function.
Article in Journal of cellular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
The trial behind it
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Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- GutMGene-Guided Peripheral Blood Transcriptomics Identifies an FLNA-Associated Host-Gene Signal in Diabetic Retinopathy.International journal of molecular sciences · 2026Article
- The potential of ARL4C and its-mediated genes in atherosclerosis and agent development.Frontiers in pharmacology · 2025Review
- Charting the importance of filamin A posttranslational modifications.The Biochemical journal · 2024Review
- The CLDN5 gene at the blood-brain barrier in health and disease.Fluids and barriers of the CNS · 2023Review
- Actin cytoskeleton in angiogenesis.Biology open · 2022Review
- RhoGDI2-Mediated Rac1 Recruitment to Filamin A Enhances Rac1 Activity and Promotes Invasive Abilities of Gastric Cancer Cells.Cancers · 2022Article
- The Role of RASGRP2 in Vascular Endothelial Cells-A Mini Review.International journal of molecular sciences · 2021Review
- Review
- Filamin A Regulates Cardiovascular Remodeling.International journal of molecular sciences · 2021Review
- RasGRP2 inhibits glyceraldehyde-derived toxic advanced glycation end-products from inducing permeability in vascular endothelial cells.Scientific reports · 2021Article
- Exploration of Oxygen-Induced Retinopathy Model to Discover New Therapeutic Drug Targets in Retinopathies.Frontiers in pharmacology · 2020Review
- The inhibition of Bax activation-induced apoptosis by RasGRP2 via R-Ras-PI3K-Akt signaling pathway in the endothelial cells.Scientific reports · 2019Article
- Filamin-A as a Balance between Erk/Smad Activities During Cardiac Valve Development.Anatomical record (Hoboken, N.J. : 2007) · 2019Article
- Involvement of Ubiquitin-Editing Protein A20 in Modulating Inflammation in Rat Cochlea Associated with Silver Nanoparticle-Induced CD68 Upregulation and TLR4 Activation.Nanoscale research letters · 2016Article
- Lack of R-Ras Leads to Increased Vascular Permeability in Ischemic Retinopathy.Investigative ophthalmology & visual science · 2016Article
- Factors regulating capillary remodeling in a reversible model of inflammatory corneal angiogenesis.Scientific reports · 2016Article
- MicroRNAs as key regulators of GTPase-mediated apical actin reorganization in multiciliated epithelia.Small GTPases · 2016Review
- Dephosphorylation of Y685-VE-Cadherin Involved in Pulmonary Microvascular Endothelial Barrier Injury Induced by Angiotensin II.Mediators of inflammation · 2016Article
- miR-34/449 control apical actin network formation during multiciliogenesis through small GTPase pathways.Nature communications · 2015Article
- Increased Infiltration of Extra-Cardiac Cells in Myxomatous Valve Disease.Journal of cardiovascular development and disease · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The molecular mechanisms regulating vascular barrier integrity remain incompletely elucidated. We have previously reported an association between the GTPase R-Ras and repeat 3 of Filamin A (FLNa). Loss of FLNa has been linked to increased vascular permeability. We sought to determine whether FLNa's association with R-Ras affects endothelial barrier function. We report that in endothelial cells endogenous R-Ras interacts with endogenous FLNa as determined by co-immunoprecipitations and pulldowns with the FLNa-GST fusion protein repeats 1-10. Deletion of FLNa repeat 3 (FLNaΔ3) abrogated this interaction. In these cells FLNa and R-Ras co-localize at the plasma membrane. Knockdown of R-Ras and/or FLNa by siRNA promotes vascular permeability, as determined by TransEndothelial Electrical Resistance and FITC-dextran transwell assays. Re-expression of FLNa restored endothelial barrier function in cells lacking FLNa whereas re-expression of FLNaΔ3 did not. Immunostaining for VE-Cadherin in cells with knocked down R-Ras and FLNa demonstrated a disorganization of VE-Cadherin at adherens junctions. Loss of R-Ras and FLNa or blocking R-Ras function via GGTI-2133, a selective R-Ras inhibitor, induced vascular permeability and increased phosphorylation of VE-Cadherin (Y731) and Src (Y416). Expression of dominant negative R-Ras promoted vascular permeability that was blocked by the Src inhibitor PP2. These findings demonstrate that maintaining endothelial barrier function is dependent upon active R-Ras and association between R-Ras and FLNa and that loss of this interaction promotes VE-Cadherin phosphorylation and changes in downstream effectors that lead to endothelial leakiness.
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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.