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- W2066002502 abstract "Insulin plays a central role in the regulation of vertebrate metabolism. The hormone, the post-translational product of a single-chain precursor, is a globular protein containing two chains, A (21 residues) and B (30 residues). Recent advances in human genetics have identified dominant mutations in the insulin gene causing permanent neonatal-onset DM(2) (1-4). The mutations are predicted to block folding of the precursor in the ER of pancreatic beta-cells. Although expression of the wild-type allele would in other circumstances be sufficient to maintain homeostasis, studies of a corresponding mouse model (5-7) suggest that the misfolded variant perturbs wild-type biosynthesis (8, 9). Impaired beta-cell secretion is associated with ER stress, distorted organelle architecture, and cell death (10). These findings have renewed interest in insulin biosynthesis (11-13) and the structural basis of disulfide pairing (14-19). Protein evolution is constrained not only by structure and function but also by susceptibility to toxic misfolding." @default.
- W2066002502 created "2016-06-24" @default.
- W2066002502 creator A5076264613 @default.
- W2066002502 date "2009-07-01" @default.
- W2066002502 modified "2023-10-02" @default.
- W2066002502 title "Proinsulin and the Genetics of Diabetes Mellitus" @default.
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- W2066002502 doi "https://doi.org/10.1074/jbc.r109.009936" @default.
- W2066002502 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2740536" @default.
- W2066002502 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19395706" @default.
- W2066002502 hasPublicationYear "2009" @default.
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