ArticleProceedings of the National Academy of Sciences of the United States of America2000
Diabetes-associated mutations in a beta-cell transcription factor destabilize an antiparallel "mini-zipper" in a dimerization interface.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.
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5 citing papers in PubMed, 14 citations in OpenAlex.
- Why all MODY variants in transcription factor genes are dominantly inherited.Frontiers in genetics · 2025Article
- Developmental disorders caused by haploinsufficiency of transcriptional regulators: a perspective based on cell fate determination.Biology open · 2022Article
- Identification and functional analysis of c.422_423InsT, a novel mutation of theMolecular genetics & genomic medicine · 2017Article
- Functional analyses of the mutation nt-128 T→G in the hepatocyte nuclear factor-1α promoter region in Chinese diabetes pedigrees.Diabetic medicine : a journal of the British Diabetic Association · 2012Article
- The genetics of type 2 diabetes: what have we learned from GWAS?Annals of the New York Academy of Sciences · 2010Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maturity-onset diabetes of the young, a monogenic form of Type II diabetes mellitus, is most commonly caused by mutations in hepatic nuclear factor 1alpha (HNF-1alpha). Here, the dimerization motif of HNF-1alpha is shown to form an intermolecular four-helix bundle. One face contains an antiparallel coiled coil whereas the other contains splayed alpha-helices. The "mini-zipper" is complementary in structure and symmetry to the top surface of a transcriptional coactivator (dimerization cofactor of homeodomains). The bundle is destabilized by a subset of mutations associated with maturity-onset diabetes of the young. Impaired dimerization of a beta-cell transcription factor thus provides a molecular mechanism of metabolic deregulation in diabetes mellitus.
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