ArticleCurrent biology : CB2017
VE-Cadherin Phosphorylation Regulates Endothelial Fluid Shear Stress Responses through the Polarity Protein LGN.
Article in Current biology : CB, 2017. 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 42 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.
The trial behind it
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
42 citing papers in PubMed, 84 citations in OpenAlex.
- Endothelial Epac1 facilitates YAP/TAZ controlled melanoma growth and angiogenesis.Angiogenesis · 2026Article
- Trimethylamine N-oxide (TMAO) disrupts endothelial junction integrity through VE-cadherin Tyr658 phosphorylation in vitro.Archives of toxicology · 2026Article
- Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- Elevated hydrostatic pressure destabilizes VE-cadherin junctions in a time and shear stress dependent manner: An endothelium-on-chip study.APL bioengineering · 2025Article
- Distinct VE-cadherin serine and tyrosine phosphorylation sites and their role for inflammation-induced vascular permeability in vivo.Cellular and molecular life sciences : CMLS · 2025Article
- Pericyte and Endothelial Cell Responses within Murine Cerebral Capillaries After Blood Flow Cessation.bioRxiv : the preprint server for biology · 2025Article
- Acoustic-pressure-driven ultrasonic activation of the mechanosensitive receptor RET and of cell proliferation in colonic tissue.Nature biomedical engineering · 2025Article
- Dysfunctional mechanotransduction regulates the progression of PIK3CA-driven vascular malformations.APL bioengineering · 2025Article
- FYN regulates aqueous humor outflow and IOP through the phosphorylation of VE-CADHERIN.Nature communications · 2025Article
- Dysfunctional mechanotransduction regulates the progression of PIK3CA-driven vascular malformations.bioRxiv : the preprint server for biology · 2024Article
- Integrating molecular and cellular components of endothelial shear stress mechanotransduction.American journal of physiology. Heart and circulatory physiology · 2024Review
- Controversy in mechanotransduction - the role of endothelial cell-cell junctions in fluid shear stress sensing.Journal of cell science · 2024Article
- Endothelial γ-protocadherins inhibit KLF2 and KLF4 to promote atherosclerosis.Nature cardiovascular research · 2024Article
- Molecular Mechanisms Regulating Vascular Endothelial Permeability.International journal of molecular sciences · 2024Review
- Article
- Endothelial mechanobiology in atherosclerosis.Cardiovascular research · 2023Review
- The VE-cadherin/AmotL2 mechanosensory pathway suppresses aortic inflammation and the formation of abdominal aortic aneurysms.Nature cardiovascular research · 2023Article
- Mechanisms of endothelial flow sensing.Nature cardiovascular research · 2023Review
- The role of blood flow in vessel remodeling and its regulatory mechanism during developmental angiogenesis.Cellular and molecular life sciences : CMLS · 2023Review
- Vascular mechanotransduction.Physiological reviews · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
Fluid shear stress due to blood flow on the vascular endothelium regulates blood vessel development, remodeling, physiology, and pathology [1, 2]. A complex consisting of PECAM-1, VE-cadherin, and vascular endothelial growth factor receptors (VEGFRs) that resides at endothelial cell-cell junctions transduces signals important for flow-dependent vasodilation, blood vessel remodeling, and atherosclerosis. PECAM-1 transduces forces to activate src family kinases (SFKs), which phosphorylate and transactivate VEGFRs [3-5]. By contrast, VE-cadherin functions as an adaptor that interacts with VEGFRs through their respective cytoplasmic domains and promotes VEGFR activation in flow [6]. Indeed, shear stress triggers rapid increases in force across PECAM-1 but decreases the force across VE-cadherin, in close association with downstream signaling [5]. Interestingly, VE-cadherin cytoplasmic tyrosine Y658 can be phosphorylated by SFKs [7], which is maximally induced by low shear stress in vitro and in vivo [8]. These considerations prompted us to address the involvement of VE-cadherin cytoplasmic tyrosines in flow sensing. We found that phosphorylation of a small pool of VE-cadherin on Y658 is essential for flow sensing through the junctional complex. Y658 phosphorylation induces dissociation of p120ctn, which allows binding of the polarity protein LGN. LGN is then required for multiple flow responses in vitro and in vivo, including activation of inflammatory signaling at regions of disturbed flow, and flow-dependent vascular remodeling. Thus, endothelial flow mechanotransduction through the junctional complex is mediated by a specific pool of VE-cadherin that is phosphorylated on Y658 and bound to LGN.
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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.