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Article

No evidence for mutations in a putative beta-cell ATP-sensitive K+ channel subunit in MODY, NIDDM, or GDM.

Diabetes - 1 May 1995

Zhang Y, Warren-Perry M, Sakura H, Adelman J, Stoffel M, Bell G I, Ashcroft F M, Turner R C

Abstract excerpt

The beta-cell ATP-sensitive K+ (K-ATP) channel has a major role in glucose-induced insulin secretion. Screening the entire coding sequence of the gene for a putative beta-cell K-ATP channel subunit, K-ATP2, with single-strand conformation polymorphism did not show any mutations associated with diabetes in white Caucasian diabetic patients, including five pedigrees with maturity onset diabetes of the young (MODY),...

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Identifiers

PMID: 7729622
DOI: 10.2337/diab.44.5.597

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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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No evidence for mutations in a putative beta-cell ATP-sensitive K+ channel subunit in MODY, NIDDM, or GDM.PMID 7729622Read ↗

No evidence for mutations in a putative subunit of the beta-cell ATP-sensitive potassium channel (K-ATP channel) in Japanese NIDDM patients.Semantic proximity Read ↗

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Single-strand conformation polymorphism analysis of the glucose transporter gene GLUT1 in maturity-onset diabetes of the young.Semantic proximity Read ↗

Search for a third susceptibility gene for maturity-onset diabetes of the young. Studies with eleven candidate genes.Semantic proximity Read ↗

Sequence variants in the pancreatic islet beta-cell inwardly rectifying K+ channel Kir6.2 (Bir) gene: identification and lack of role in Caucasian patients with NIDDM.Semantic proximity Read ↗

Candidate gene studies in pedigrees with maturity-onset diabetes of the young not linked with glucokinase.Semantic proximity Read ↗

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The beta cell glucokinase promoter variant is an unlikely risk factor for diabetes mellitus. Diabetes Incidence Study in Sweden (DISS).Semantic proximity Read ↗

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