ArticleThe Journal of cell biology1998
Acute loss of cell-cell communication caused by G protein-coupled receptors: a critical role for c-Src.
Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 108 citations in OpenAlex.
- The relationship between substrate topography and stem cell differentiation in the musculoskeletal system.Cellular and molecular life sciences : CMLS · 2019Review
- The Role of Gap Junction-Mediated Endothelial Cell-Cell Interaction in the Crosstalk between Inflammation and Blood Coagulation.International journal of molecular sciences · 2017Review
- Regulation of cardiac gap junctions by protein phosphatases.Journal of molecular and cellular cardiology · 2017Review
- Molecular mechanisms regulating formation, trafficking and processing of annular gap junctions.BMC cell biology · 2016Review
- Connexin43 phosphorylation by PKC and MAPK signals VEGF-mediated gap junction internalization.Molecular biology of the cell · 2015Article
- TC-PTP directly interacts with connexin43 to regulate gap junction intercellular communication.Journal of cell science · 2014Article
- Osteoblastic protein tyrosine phosphatases inhibition and connexin 43 phosphorylation by alendronate.Experimental cell research · 2014Article
- Degradation of connexins and gap junctions.FEBS letters · 2014Review
- Managing the complexity of communication: regulation of gap junctions by post-translational modification.Frontiers in pharmacology · 2013Review
- Two tyrosine-based sorting signals in the Cx43 C-terminus cooperate to mediate gap junction endocytosis.Molecular biology of the cell · 2013Article
- Proteins and mechanisms regulating gap-junction assembly, internalization, and degradation.Physiology (Bethesda, Md.) · 2013Review
- Degradation of endocytosed gap junctions by autophagosomal and endo-/lysosomal pathways: a perspective.The Journal of membrane biology · 2012Review
- Gap junctions.Comprehensive Physiology · 2012Review
- Connexin43 cardiac gap junction remodeling: lessons from genetically engineered murine models.The Journal of membrane biology · 2012Review
- Internalized gap junctions are degraded by autophagy.Autophagy · 2012Article
- Gap junctions and blood-tissue barriers.Advances in experimental medicine and biology · 2012Article
- Phosphatase-resistant gap junctions inhibit pathological remodeling and prevent arrhythmias.Circulation research · 2011Article
- Mechanisms of gap junction traffic in health and disease.Journal of cardiovascular pharmacology · 2009Review
- Connexins: a myriad of functions extending beyond assembly of gap junction channels.Cell communication and signaling : CCS · 2009Article
- Connexin 43 gap junction plaque endocytosis implies molecular remodelling of ZO-1 and c-Src partners.Communicative & integrative biology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gap junctions mediate cell-cell communication in almost all tissues, but little is known about their regulation by physiological stimuli. Using a novel single-electrode technique, together with dye coupling studies, we show that in cells expressing gap junction protein connexin43, cell-cell communication is rapidly disrupted by G protein-coupled receptor agonists, notably lysophosphatidic acid, thrombin, and neuropeptides. In the continuous presence of agonist, junctional communication fully recovers within 1-2 h of receptor stimulation. In contrast, a desensitization-defective G protein-coupled receptor mediates prolonged uncoupling, indicating that recovery of communication is controlled, at least in part, by receptor desensitization. Agonist-induced gap junction closure consistently follows inositol lipid breakdown and membrane depolarization and coincides with Rho-mediated cytoskeletal remodeling. However, we find that gap junction closure is independent of Ca2+, protein kinase C, mitogen-activated protein kinase, or membrane potential, and requires neither Rho nor Ras activation. Gap junction closure is prevented by tyrphostins, by dominant-negative c-Src, and in Src-deficient cells. Thus, G protein-coupled receptors use a Src tyrosine kinase pathway to transiently inhibit connexin43-based cell-cell communication.
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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 Socratic graph.