ArticleThe Journal of experimental medicine2014
Evidence of a common mechanism of disassembly of adherens junctions through Gα13 targeting of VE-cadherin.
Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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Who cites it
43 citing papers in PubMed, 72 citations in OpenAlex.
- Anisodine hydrobromide targets matk and prevents delayed rtPA thrombolysis-induced vasogenic cerebral edema in ischemic stroke.Nature communications · 2026Article
- Junctions, Transporters, and Interactions of Endothelial Cells: Regulation by Ethanol.International journal of molecular sciences · 2026Review
- 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
- Vascular inflammaging: Endothelial CEACAM1 expression is upregulated by TNF-α via independent activation of NF-κB and β-catenin signaling.Aging cell · 2025Article
- Ubiquitin ligase CHFR mediated degradation of VE-cadherin through ubiquitylation disrupts endothelial adherens junctions.Nature communications · 2023Article
- Adipsin alleviates cardiac microvascular injury in diabetic cardiomyopathy through Csk-dependent signaling mechanism.BMC medicine · 2023Article
- The Role of Txnip in Mediating Low-Magnesium-Driven Endothelial Dysfunction.International journal of molecular sciences · 2023Article
- TAK1 is essential for endothelial barrier maintenance and repair after lung vascular injury.Molecular biology of the cell · 2022Article
- Gα13 loss in Kras/Tp53 mouse model of pancreatic tumorigenesis promotes tumors susceptible to rapamycin.Cell reports · 2022Article
- GαFrontiers in cell and developmental biology · 2022Review
- Enhanced endothelial barrier function by monoclonal antibody activation of vascular endothelial cadherin.American journal of physiology. Heart and circulatory physiology · 2021Article
- YAP expression in endothelial cells prevents ventilator-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Protein tyrosine phosphatases in cell adhesion.The Biochemical journal · 2021Review
- Compensatory increase of VE-cadherin expression through ETS1 regulates endothelial barrier function in response to TNFα.Cellular and molecular life sciences : CMLS · 2020Article
- Phospholipase D2 restores endothelial barrier function by promoting PTPN14-mediated VE-cadherin dephosphorylation.The Journal of biological chemistry · 2020Article
- Contrasting effects of stored allogeneic red blood cells and their supernatants on permeability and inflammatory responses in human pulmonary endothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Analysis of biological networks in the endothelium with biomimetic microsystem platform.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- VE-PTP stabilizes VE-cadherin junctions and the endothelial barrier via a phosphatase-independent mechanism.The Journal of cell biology · 2019Article
- Multiplexed, high-throughput measurements of cell contraction and endothelial barrier function.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- The Ric-8A/Gα13/FAK signalling cascade controls focal adhesion formation during neural crest cell migration inDevelopment (Cambridge, England) · 2018Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
The heterotrimeric G protein Gα13 transduces signals from G protein-coupled receptors (GPCRs) to induce cell spreading, differentiation, migration, and cell polarity. Here, we describe a novel GPCR-independent function of Gα13 in regulating the stability of endothelial cell adherens junctions (AJs). We observed that the oxidant H2O2, which is released in response to multiple proinflammatory mediators, induced the interaction of Gα13 with VE-cadherin. Gα13 binding to VE-cadherin in turn induced Src activation and VE-cadherin phosphorylation at Tyr 658, the p120-catenin binding site thought to be responsible for VE-cadherin internalization. Inhibition of Gα13-VE-cadherin interaction using an interfering peptide derived from the Gα13 binding motif on VE-cadherin abrogated the disruption of AJs in response to inflammatory mediators. These studies identify a unique role of Gα13 binding to VE-cadherin in mediating VE-cadherin internalization and endothelial barrier disruption and inflammation.
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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.