ArticleExperimental cell research2013
Phosphorylation of connexin43 on S279/282 may contribute to laminopathy-associated conduction defects.
Article in Experimental cell research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Cardiac Fibroblasts: Helping or Hurting.Genes · 2025Review
- Role of Nuclear Lamins in the Regulation of the Genome: Focus on CardioLaminopathy.Sub-cellular biochemistry · 2025Review
- Preclinical Advances of Therapies for Laminopathies.Journal of clinical medicine · 2021Review
- Phenotypic Variability in iPSC-Induced Cardiomyocytes and Cardiac Fibroblasts Carrying DiverseFrontiers in physiology · 2021Article
- Updated clinical overview on cardiac laminopathies: an electrical and mechanical disease.Nucleus (Austin, Tex.) · 2018Review
- Role of Lamin A/C Gene Mutations in the Signaling Defects Leading to Cardiomyopathies.Frontiers in physiology · 2018Review
- Lamin A/C Cardiomyopathies: Current Understanding and Novel Treatment Strategies.Current treatment options in cardiovascular medicine · 2017Review
- Current insights into LMNA cardiomyopathies: Existing models and missing LINCs.Nucleus (Austin, Tex.) · 2017Review
- Connexin 43 is an emerging therapeutic target in ischemia/reperfusion injury, cardioprotection and neuroprotection.Pharmacology & therapeutics · 2015Review
- MicroRNA-23a participates in estrogen deficiency induced gap junction remodeling of rats by targeting GJA1.International journal of biological sciences · 2015Article
- AFM single-cell force spectroscopy links altered nuclear and cytoskeletal mechanics to defective cell adhesion in cardiac myocytes with a nuclear lamin mutation.Nucleus (Austin, Tex.) · 2015Article
- Specific Cx43 phosphorylation events regulate gap junction turnover in vivo.FEBS letters · 2014Review
- Cardiomyocyte FGF signaling is required for Cx43 phosphorylation and cardiac gap junction maintenance.Experimental cell research · 2013Article
- Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
An understanding of the molecular mechanism behind the arrhythmic phenotype associated with laminopathies has yet to emerge. A-type lamins have been shown to interact and sequester activated phospho-ERK1/2(pERK1/2) at the nucleus. The gap junction protein connexin43 (Cx43) can be phosphorylated by pERK1/2 on S279/282 (pS279/282), inhibiting intercellular communication. We hypothesized that without A-type lamins, pS279/282 Cx43 will increase due to inappropriate phosphorylation by pERK1/2, resulting in decreased gap junction function. We observed a 1.6-fold increase in pS279/282 Cx43 levels in Lmna(-/-) mouse embryonic fibroblasts (MEFs) compared to Lmna(+/+), and 1.8-fold more pERK1/2 co-precipitated from Lmna(-/-) MEFs with Cx43 antibodies. We found a 3-fold increase in the fraction of non-nuclear pERK1/2 and a concomitant 2-fold increase in the fraction of pS279/282 Cx43 in Lmna(-/-) MEFs by immunofluorescence. In an assay of gap junctional function, Lmna(-/-) MEFs transferred dye to 60% fewer partners compared to Lmna(+/+) controls. These results are mirrored in 5-6 week-old Lmna(-/-) mice compared to their Lmna(+/+) littermates as we detect increased pS279/282 Cx43 in gap junctions by immunofluorescence and 1.7-fold increased levels by immunoblot. We conclude that increased pS279/282 Cx43 in the Lmna(-/-) background results in decreased cell communication and may contribute to the arrhythmic pathology in vivo.
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