ArticleAmerican journal of physiology. Endocrinology and metabolism2016
Extracellular CADM1 interactions influence insulin secretion by rat and human islet β-cells and promote clustering of syntaxin-1.
Article in American journal of physiology. Endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- MicroRNA-Driven Regulation of β-Cell Function in Type 2 Diabetes: Molecular Mechanisms, Network Insights, and Translational Perspectives.Acta physiologica (Oxford, England) · 2026Review
- Dysregulation of the miR-4286 in diabetic kidney disease and its role in inflammatory response.Diabetology & metabolic syndrome · 2026Article
- Low Expression of Cell Adhesion Molecule 1 in Resected Gastroenteropancreatic Neuroendocrine Tumors: Relationship With Lymph Node and Distant Metastasis.Pathology international · 2026Article
- Network-based insights into miRNA regulation of β-cell insulin secretion in type 2 diabetes.iScience · 2025Article
- Developmental programming: Differing impact of prenatal testosterone and prenatal bisphenol-A -treatment on hepatic methylome in female sheep.Molecular and cellular endocrinology · 2025Article
- MicroRNA 375 and diabetes: A key regulator of β cell function and a promising non-invasive biomarker.World journal of diabetes · 2025Review
- Chemical mapping of the surface interactome of PIEZO1 identifies CADM1 as a modulator of channel inactivation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Somatic mutations of CADM1 in aldosterone-producing adenomas and gap junction-dependent regulation of aldosterone production.Nature genetics · 2023Article
- Persistent coxsackievirus B1 infection triggers extensive changes in the transcriptome of human pancreatic ductal cells.iScience · 2022Article
- Divalent Metal Transporter 1 Knock-Down Modulates IL-1β Mediated Pancreatic Beta-Cell Pro-Apoptotic Signaling Pathways through the Autophagic Machinery.International journal of molecular sciences · 2021Article
- miR-375 Promotes Pancreatic DifferentiationStem cells international · 2021Article
- Recent Insights into Beta-cell Exocytosis in Type 2 Diabetes.Journal of molecular biology · 2020Review
- Decreased intracellular granule movement and glucagon secretion in pancreatic α cells attached to superior cervical ganglion neurites.Molecular and cellular biochemistry · 2018Article
- Cell-sized lipid vesicles for cell-cell synaptic therapies.Technology · 2017Article
- Changes in pancreatic histology, insulin secretion and oxidative status in diabetic rats following treatment with Ficus deltoidea and vitexin.BMC complementary and alternative medicine · 2017Article
- Exocytosis proteins as novel targets for diabetes prevention and/or remediation?American journal of physiology. Regulatory, integrative and comparative physiology · 2017Review
- Article
- Nuclear Export of FoxO1 Is Associated with ERK Signaling in β-Cells Lacking Insulin Receptors.The Journal of biological chemistry · 2016Article
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7 authors.
Funding
Abstract
Contact between β-cells is necessary for their normal function. Identification of the proteins mediating the effects of β-cell-to-β-cell contact is a necessary step toward gaining a full understanding of the determinants of β-cell function and insulin secretion. The secretory machinery of the β-cells is nearly identical to that of central nervous system (CNS) synapses, and we hypothesize that the transcellular protein interactions that drive maturation of the two secretory machineries upon contact of one cell (or neural process) with another are also highly similar. Two such transcellular interactions, important for both synaptic and β-cell function, have been identified: EphA/ephrin-A and neuroligin/neurexin. Here, we tested the role of another synaptic cleft protein, CADM1, in insulinoma cells and in rat and human islet β-cells. We found that CADM1 is a predominant CADM isoform in β-cells. In INS-1 cells and primary β-cells, CADM1 constrains insulin secretion, and its expression decreases after prolonged glucose stimulation. Using a coculture model, we found that CADM1 also influences insulin secretion in a transcellular manner. We asked whether extracellular CADM1 interactions exert their influence via the same mechanisms by which they influence neurotransmitter exocytosis. Our results suggest that, as in the CNS, CADM1 interactions drive exocytic site assembly and promote actin network formation. These results support the broader hypothesis that the effects of cell-cell contact on β-cell maturation and function are mediated by the same extracellular protein interactions that drive the formation of the presynaptic exocytic machinery. These interactions may be therapeutic targets for reversing β-cell dysfunction in diabetes.
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