ArticlePloS one2016
A Variant of GJD2, Encoding for Connexin 36, Alters the Function of Insulin Producing β-Cells.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Association Between Polymorphisms of 4 Common Genes and High Myopia Risk: A Comprehensive Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2026Pooled it
- Unveiling Genetic Markers for Milk Yield in Xinjiang Donkeys: A Genome-Wide Association Study and Kompetitive Allele-Specific PCR-Based Approach.International journal of molecular sciences · 2025Article
- Restoring connexin-36 function in diabetogenic environments precludes mouse and human islet dysfunction.The Journal of physiology · 2023Article
- Is type 2 diabetes mellitus another intercellular junction-related disorder?Experimental biology and medicine (Maywood, N.J.) · 2022Article
- The Role of GJD2(Cx36) in Refractive Error Development.Investigative ophthalmology & visual science · 2022Review
- Modulation of Gap Junction Coupling Within the Islet of Langerhans During the Development of Type 1 Diabetes.Frontiers in physiology · 2022Article
- The effects of beta-cell mass and function, intercellular coupling, and islet synchrony on [Formula: see text] dynamics.Scientific reports · 2021Article
- Caloric restriction recovers impaired β-cell-β-cell gap junction coupling, calcium oscillation coordination, and insulin secretion in prediabetic mice.American journal of physiology. Endocrinology and metabolism · 2020Article
- Heterozygous connexin 50 mutation affects metabolic syndrome attributes in spontaneously hypertensive rat.Lipids in health and disease · 2016Article
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signalling through gap junctions contributes to control insulin secretion and, thus, blood glucose levels. Gap junctions of the insulin-producing β-cells are made of connexin 36 (Cx36), which is encoded by the GJD2 gene. Cx36-null mice feature alterations mimicking those observed in type 2 diabetes (T2D). GJD2 is also expressed in neurons, which share a number of common features with pancreatic β-cells. Given that a synonymous exonic single nucleotide polymorphism of human Cx36 (SNP rs3743123) associates with altered function of central neurons in a subset of epileptic patients, we investigated whether this SNP also caused alterations of β-cell function. Transfection of rs3743123 cDNA in connexin-lacking HeLa cells resulted in altered formation of gap junction plaques and cell coupling, as compared to those induced by wild type (WT) GJD2 cDNA. Transgenic mice expressing the very same cDNAs under an insulin promoter revealed that SNP rs3743123 expression consistently lead to a post-natal reduction of islet Cx36 levels and β-cell survival, resulting in hyperglycemia in selected lines. These changes were not observed in sex- and age-matched controls expressing WT hCx36. The variant GJD2 only marginally associated to heterogeneous populations of diabetic patients. The data document that a silent polymorphism of GJD2 is associated with altered β-cell function, presumably contributing to T2D pathogenesis.
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