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Article

Defective trafficking and function of KATP channels caused by a sulfonylurea receptor 1 mutation associated with persistent hyperinsulinemic hypoglycemia of infancy.

Proceedings of the National Academy of Sciences of the United States of America - 27 Feb 2001

Cartier E A, Conti L R, Vandenberg C A, Shyng S L

Abstract excerpt

The ATP-sensitive potassium channel (K(ATP)) regulates insulin secretion in pancreatic beta cells. Loss of functional K(ATP) channels because of mutations in either the SUR1 or Kir6.2 channel subunit causes persistent hyperinsulinemic hypoglycemia of infancy (PHHI). We investigated the molecular mechanism by which a single phenylalanine deletion in SUR1 (DeltaF1388) causes PHHI. Previous studies have shown that...

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Share to ATP-Binding Cassette Transporters
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Membrane Potentials

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Source

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Identifiers

PMID: 11226335
DOI: 10.1073/pnas.051499698
PMCID: PMC30234

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

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Defective trafficking and function of KATP channels caused by a sulfonylurea receptor 1 mutation associated with persistent hyperinsulinemic hypoglycemia of infancy.PMID 11226335Read ↗

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