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- W2067097574 abstract "Clec16a has been identified as a disease susceptibility gene for type 1 diabetes, multiple sclerosis, and adrenal dysfunction, but its function is unknown. Here we report that Clec16a is a membrane-associated endosomal protein that interacts with E3 ubiquitin ligase Nrdp1. Loss of Clec16a leads to an increase in the Nrdp1 target Parkin, a master regulator of mitophagy. Islets from mice with pancreas-specific deletion of Clec16a have abnormal mitochondria with reduced oxygen consumption and ATP concentration, both of which are required for normal β cell function. Indeed, pancreatic Clec16a is required for normal glucose-stimulated insulin release. Moreover, patients harboring a diabetogenic SNP in the Clec16a gene have reduced islet Clec16a expression and reduced insulin secretion. Thus, Clec16a controls β cell function and prevents diabetes by controlling mitophagy. This pathway could be targeted for prevention and control of diabetes and may extend to the pathogenesis of other Clec16a- and Parkin-associated diseases." @default.
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- W2067097574 date "2014-06-01" @default.
- W2067097574 modified "2023-10-15" @default.
- W2067097574 title "The Diabetes Susceptibility Gene Clec16a Regulates Mitophagy" @default.
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- W2067097574 doi "https://doi.org/10.1016/j.cell.2014.05.016" @default.
- W2067097574 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4184276" @default.
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- W2067097574 hasPublicationYear "2014" @default.
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