Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Sulfonylureas correct trafficking defects of disease-causing ATP-sensitive potassium channels by binding to the channel complex.

The Journal of biological chemistry - 3 Nov 2006

Yan Fei-Fei, Casey Jillene, Shyng Show-Ling

Abstract excerpt

ATP-sensitive potassium (K(ATP)) channels mediate glucose-induced insulin secretion by coupling metabolic signals to beta-cell membrane potential and the secretory machinery. Reduced K(ATP) channel expression caused by mutations in the channel proteins: sulfonylurea receptor 1 (SUR1) and Kir6.2, results in loss of channel function as seen in congenital hyperinsulinism. Previously, we reported that sulfonylureas,...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Adenosine Triphosphate
Share to Chlorocebus aethiops

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Disease

Share to Electrophysiology

Share to Patch-Clamp Techniques

Share to Potassium Channels

Share to Protein Subunits

Share to Sulfonylurea Compounds

Source

Identifiers

PMID: 16956886
DOI: 10.1074/jbc.M605195200

Provenance

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.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Sulfonylureas correct trafficking defects of disease-causing ATP-sensitive potassium channels by binding to the channel complex.PMID 16956886Read ↗

Sulfonylureas correct trafficking defects of ATP-sensitive potassium channels caused by mutations in the sulfonylurea receptor.Semantic proximity Read ↗

Pharmacological Correction of Trafficking Defects in ATP-sensitive Potassium Channels Caused by Sulfonylurea Receptor 1 Mutations.Semantic proximity Read ↗

Sulfonylurea receptor 1 mutations that cause opposite insulin secretion defects with chemical chaperone exposure.Semantic proximity Read ↗

Identification of a familial hyperinsulinism-causing mutation in the sulfonylurea receptor 1 that prevents normal trafficking and function of KATP channels.Semantic proximity Read ↗

Congenital Hyperinsulinism–Associated <i>ABCC8</i> Mutations That Cause Defective Trafficking of ATP-Sensitive K+ ChannelsSemantic proximity Read ↗

Modulation of the trafficking efficiency and functional properties of ATP-sensitive potassium channels through a single amino acid in the sulfonylurea receptor.Semantic proximity Read ↗

Identification and Rescue of Congenital Hyperinsulinism-Associated <i>ABCC8</i> Mutations that Impair K <sub>ATP</sub> Channel TraffickingSemantic proximity Read ↗

A role of the sulfonylurea receptor 1 in endocytic trafficking of ATP-sensitive potassium channels.Semantic proximity Read ↗

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

Engineered Kir6.2 mutations that correct the trafficking defect of K(ATP) channels caused by specific SUR1 mutations.Semantic proximity Read ↗

Trafficking of ATP-sensitive potassium channels in health and disease.Semantic proximity Read ↗

Carbamazepine as a novel small molecule corrector of trafficking-impaired ATP-sensitive potassium channels identified in congenital hyperinsulinism.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.