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Article

The ATP-sensitive K(+) channel ABCC8 S1369A type 2 diabetes risk variant increases MgATPase activity.

Diabetes - 1 Jan 2012

Fatehi Mohammad, Raja Mobeen, Carter Christian, Soliman Daniel, Holt Andrew, Light Peter E

Abstract excerpt

Pancreatic β-cell ATP-sensitive K(+) (K(ATP)) channels are composed of Kir6.2 and SUR1 subunits encoded by the KCNJ11 and ABCC8 genes, respectively. Although rare monogenic activating mutations in these genes cause overt neonatal diabetes, the common variants E23K (KCNJ11) and S1369A (ABCC8) form a tightly heritable haplotype that is associated with an increased susceptibility to type 2 diabetes (T2D) risk....

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Share to Adenosine Triphosphate
Share to Alanine
Share to ATP-Binding Cassette Transporters

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to KATP Channels

Share to Potassium Channels, Inwardly Rectifying

Share to Receptors, Drug

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Share to Sulfonylurea Receptors

Source

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Identifiers

PMID: 22187380
DOI: 10.2337/db11-0371
PMCID: PMC3237651

Genes

ABCC8
KCNJ11

Variants

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.

Related research

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Research trail→

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The ATP-sensitive K(+) channel ABCC8 S1369A type 2 diabetes risk variant increases MgATPase activity.PMID 22187380Read ↗

Compound heterozygous mutations in the SUR1 (ABCC 8) subunit of pancreatic K(ATP) channels cause neonatal diabetes by perturbing the coupling between Kir6.2 and SUR1 subunits.Semantic proximity Read ↗

Coexpression of the type 2 diabetes susceptibility gene variants KCNJ11 E23K and ABCC8 S1369A alter the ATP and sulfonylurea sensitivities of the ATP-sensitive K(+) channel.Semantic proximity Read ↗

A rare mutation in ABCC8/SUR1 leading to altered ATP-sensitive K+ channel activity and beta-cell glucose sensing is associated with type 2 diabetes in adults.Semantic proximity Read ↗

Adjacent mutations in the gating loop of Kir6.2 produce neonatal diabetes and hyperinsulinismSemantic proximity Read ↗

Molecular biology of K(ATP) channels and implications for health and disease.Semantic proximity Read ↗

Kir6.2 mutations causing neonatal diabetes provide new insights into Kir6.2-SUR1 interactions.Semantic proximity Read ↗

Haplotype structure and genotype-phenotype correlations of the sulfonylurea receptor and the islet ATP-sensitive potassium channel gene region.Semantic proximity Read ↗

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A novel KCNJ11 mutation associated with congenital hyperinsulinism reduces the intrinsic open probability of beta-cell ATP-sensitive potassium channels.Semantic proximity Read ↗

Pharmacogenomic analysis of ATP-sensitive potassium channels coexpressing the common type 2 diabetes risk variants E23K and S1369A.Semantic proximity Read ↗

Functional effects of naturally occurring KCNJ11 mutations causing neonatal diabetes on cloned cardiac KATP channels.Semantic proximity Read ↗

The common single nucleotide polymorphism E23K in K(IR)6.2 sensitizes pancreatic beta-cell ATP-sensitive potassium channels toward activation through nucleoside diphosphates.Semantic proximity Read ↗

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