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Article

Kir6.2 mutations causing neonatal diabetes provide new insights into Kir6.2-SUR1 interactions.

The EMBO journal - 6 Jul 2005

Tammaro Paolo, Girard Christophe, Molnes Janne, Njølstad Pål R, Ashcroft Frances M

Abstract excerpt

ATP-sensitive K(+) (K(ATP)) channels, comprised of pore-forming Kir6.2 and regulatory SUR1 subunits, play a critical role in regulating insulin secretion. Binding of ATP to Kir6.2 inhibits, whereas interaction of MgATP with SUR1 activates, K(ATP) channels. We tested the functional effects of two Kir6.2 mutations (Y330C, F333I) that cause permanent neonatal diabetes mellitus, by heterologous expression in Xenopus...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 15962003
DOI: 10.1038/sj.emboj.7600715
PMCID: PMC1173155

Provenance

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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