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Article

ATP and sulfonylurea sensitivity of mutant ATP-sensitive K+ channels in neonatal diabetes: implications for pharmacogenomic therapy.

Diabetes - 1 Sept 2005

Koster Joseph C, Remedi Maria S, Dao Crystal, Nichols Colin G

Abstract excerpt

The prediction that overactivity of the pancreatic ATP-sensitive K(+) channel (K(ATP) channel) underlies reduced insulin secretion and causes a diabetic phenotype in humans has recently been borne out by genetic studies implicating "activating" mutations in the Kir6.2 subunit of K(ATP) as causal in both permanent and transient neonatal diabetes. Here we characterize the channel properties of Kir6.2 mutations that...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 16123353
DOI: 10.2337/diabetes.54.9.2645

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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ATP and sulfonylurea sensitivity of mutant ATP-sensitive K+ channels in neonatal diabetes: implications for pharmacogenomic therapy.PMID 16123353Read ↗

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

Kir6.2 mutations associated with neonatal diabetes reduce expression of ATP-sensitive K+ channels: implications in disease mechanism and sulfonylurea therapy.Semantic proximity Read ↗

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Diabetes and insulin secretion: the ATP-sensitive K+ channel (K ATP) connection.Semantic proximity Read ↗

Mutations at the same residue (R50) of Kir6.2 (KCNJ11) that cause neonatal diabetes produce different functional effects.Semantic proximity Read ↗

Neonatal diabetes caused by mutations in sulfonylurea receptor 1: interplay between expression and Mg-nucleotide gating defects of ATP-sensitive potassium channels.Semantic proximity Read ↗

Functional effects of mutations at F35 in the NH2-terminus of Kir6.2 (KCNJ11), causing neonatal diabetes, and response to sulfonylurea therapy.Semantic proximity Read ↗

A Kir6.2 mutation causing severe functional effects in vitro produces neonatal diabetes without the expected neurological complications.Semantic proximity Read ↗

An ATP-binding mutation (G334D) in KCNJ11 is associated with a sulfonylurea-insensitive form of developmental delay, epilepsy, and neonatal diabetes.Semantic proximity Read ↗

Functional effects of KCNJ11 mutations causing neonatal diabetes: enhanced activation by MgATP.Semantic proximity Read ↗

Neonatal diabetes caused by a homozygous KCNJ11 mutation demonstrates that tiny changes in ATP sensitivity markedly affect diabetes risk.Semantic proximity Read ↗

Functional analysis of six Kir6.2 (KCNJ11) mutations causing neonatal diabetes.Semantic proximity Read ↗

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