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Article

A Kir6.2 mutation causing neonatal diabetes impairs electrical activity and insulin secretion from INS-1 beta-cells.

Diabetes - 1 Nov 2006

Tarasov Andrei I, Welters Hannah J, Senkel Sabine, Ryffel Gerhart U, Hattersley Andrew T, Morgan Noel G, Ashcroft Frances M

Abstract excerpt

ATP-sensitive K(+) channels (K(ATP) channels) couple beta-cell metabolism to electrical activity and thereby play an essential role in the control of insulin secretion. Gain-of-function mutations in Kir6.2 (KCNJ11), the pore-forming subunit of this channel, cause neonatal diabetes. We investigate...

Read the complete abstract on PubMed

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Share to Adenosine Triphosphate
Share to Amino Acid Substitution
Share to Diabetes Mellitus, Type 1

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Insulin

Share to Insulin-Secreting Cells

Share to Insulin Secretion

Share to Kinetics

Share to Potassium Channels, Inwardly Rectifying

Source

Identifiers

PMID: 17065345
DOI: 10.2337/db06-0637

Genes

INS
KCNJ11

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-17065345-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

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