ArticleJournal of cell science2014
An EMMPRIN-γ-catenin-Nm23 complex drives ATP production and actomyosin contractility at endothelial junctions.
Article in Journal of cell science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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
17 citing papers in PubMed, 22 citations in OpenAlex.
- Coronary and carotid artery dysfunction and KGeroScience · 2024Article
- Activation of Nm23-H1 to suppress breast cancer metastasis via redox regulation.Experimental & molecular medicine · 2021Review
- The Potential Functional Roles of NME1 Histidine Kinase Activity in Neuroblastoma Pathogenesis.International journal of molecular sciences · 2020Article
- Characterization of Nme5-Like Gene/Protein from the Red AlgaMarine drugs · 2019Article
- Arf6-driven endocytic recycling of CD147 determines HCC malignant phenotypes.Journal of experimental & clinical cancer research : CR · 2019Article
- PKM2 regulates endothelial cell junction dynamics and angiogenesis via ATP production.Scientific reports · 2019Article
- Hypoxia tolerance in the Norrin-deficient retina and the chronically hypoxic brain studied at single-cell resolution.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Small molecule activator of Nm23/NDPK as an inhibitor of metastasis.Scientific reports · 2018Article
- Article
- The NDPK/NME superfamily: state of the art.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Beyond cell-cell adhesion: Plakoglobin and the regulation of tumorigenesis and metastasis.Oncotarget · 2017Review
- Cell-cell junctional mechanotransduction in endothelial remodeling.Cellular and molecular life sciences : CMLS · 2017Review
- Self-propelling vesicles define glycolysis as the minimal energy machinery for neuronal transport.Nature communications · 2016Article
- Glycolytic regulation of cell rearrangement in angiogenesis.Nature communications · 2016Article
- Curcumin modulates chronic myelogenous leukemia exosomes composition and affects angiogenic phenotype via exosomal miR-21.Oncotarget · 2016Article
- Basigin (CD147), a multifunctional transmembrane glycoprotein with various binding partners.Journal of biochemistry · 2016Review
- ROCK2 primes the endothelium for vascular hyperpermeability responses by raising baseline junctional tension.Vascular pharmacology · 2015Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 4 countries.
Funding
Abstract
Cell-cell adhesions are important sites through which cells experience and resist forces. In endothelial cells, these forces regulate junction dynamics and determine endothelial barrier strength. We identify the Ig superfamily member EMMPRIN (also known as basigin) as a coordinator of forces at endothelial junctions. EMMPRIN localization at junctions correlates with endothelial junction strength in different mouse vascular beds. Accordingly, EMMPRIN-deficient mice show altered junctions and increased junction permeability. Lack of EMMPRIN alters the localization and function of VE-cadherin (also known as cadherin-5) by decreasing both actomyosin contractility and tugging forces at endothelial cell junctions. EMMPRIN ensures proper actomyosin-driven maturation of competent endothelial junctions by forming a molecular complex with γ-catenin (also known as junction plakoglobin) and Nm23 (also known as NME1), a nucleoside diphosphate kinase, thereby locally providing ATP to fuel the actomyosin machinery. These results provide a novel mechanism for the regulation of actomyosin contractility at endothelial junctions and might have broader implications in biological contexts such as angiogenesis, collective migration and tissue morphogenesis by coupling compartmentalized energy production to junction assembly.
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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.