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Article

Activating mutations in Kir6.2 and neonatal diabetes: new clinical syndromes, new scientific insights, and new therapy.

Diabetes - 1 Sept 2005

Hattersley Andrew T, Ashcroft Frances M

Abstract excerpt

Closure of ATP-sensitive K(+) channels (K(ATP) channels) in response to metabolically generated ATP or binding of sulfonylurea drugs stimulates insulin release from pancreatic beta-cells. Heterozygous gain-of-function mutations in the KCJN11 gene encoding the Kir6.2 subunit of this channel are found in approximately 47% of patients diagnosed with permanent diabetes at <6 months of age. There is a striking...

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Share to Diabetes Mellitus, Type 1
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Share to Infant, Newborn

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Pancreatic function and diabetes

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Share to Potassium Channels, Inwardly Rectifying

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Identifiers

PMID: 16123337
DOI: 10.2337/diabetes.54.9.2503

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Activating mutations in Kir6.2 and neonatal diabetes: new clinical syndromes, new scientific insights, and new therapy.PMID 16123337Read ↗

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