ArticleInternational journal of molecular sciences2021
BRAF Modulates Stretch-Induced Intercellular Gap Formation through Localized Actin Reorganization.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 9 citations in OpenAlex.
- The Baraitser-Winter Cerebrofrontofacial Syndrome Recurrent R196H Variant in Cytoplasmic β-Actin Impairs Its Cellular Polymerization and Stability.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Cerebrospinal fluid mechanics across CNS barriers: from production, circulation, and clearance to mechanomedicine.Frontiers in neuroscience · 2026Review
- Uniaxial cyclic stretch regulates the expression of thrombomodulin and von Willebrand factor on endothelial cells.Blood vessels, thrombosis & hemostasis · 2025Article
- Compressive Forces Induce Epigenetic Activation of Aged Human Dermal Fibroblasts Through ERK Signaling Pathway.Aging cell · 2025Article
- BRAF Modulates the Interplay Between Cell-Cell and Cell-Extracellular Matrix Adhesions in PECAM-1-Mediated Mechanotransduction.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Mechanical forces acting on cell-cell adhesion modulate the barrier function of endothelial cells. The actively remodeled actin cytoskeleton impinges on cell-cell adhesion to counteract external forces. We applied stress on endothelial monolayers by mechanical stretch to uncover the role of BRAF in the stress-induced response. Control cells responded to external forces by organizing and stabilizing actin cables in the stretched cell junctions. This was accompanied by an increase in intercellular gap formation, which was prevented in BRAF knockdown monolayers. In the absence of BRAF, there was excess stress fiber formation due to the enhanced reorganization of actin fibers. Our findings suggest that stretch-induced intercellular gap formation, leading to a decrease in barrier function of blood vessels, can be reverted by BRAF RNAi. This is important when the endothelium experiences changes in external stresses caused by high blood pressure, leading to edema, or by immune or cancer cells in inflammation or metastasis.
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Registered trials
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