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

A novel ABCC8 (SUR1)-dependent mechanism of metabolism-excitation uncoupling.

The Journal of biological chemistry - 4 Apr 2008

Babenko Andrey P

Abstract excerpt

ATP/ADP-sensing (sulfonylurea receptor (SUR)/K(IR)6)(4) K(ATP) channels regulate the excitability of our insulin secreting and other vital cells via the differential MgATP/ADP-dependent stimulatory actions of their tissue-specific ATP-binding cassette regulatory subunits (sulfonylurea receptors), which counterbalance the nearly constant inhibitory action of ATP on the K(+) inwardly rectifying pore. Mutations in...

Read the complete abstract on PubMed

Topics

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

Share to Cell Polarity
Share to Hypoglycemic Agents
Share to Insulin Secretion

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Magnesium

Share to Potassium Channels

Share to Potassium Channels, Inwardly Rectifying

Share to Receptors, Drug

Share to Sulfonylurea Receptors

Source

Open in PubMed Open full text

Identifiers

PMID: 18281290
DOI: 10.1074/jbc.C700243200
PMCID: PMC2276369

Genes

ABCC8

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

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A novel ABCC8 (SUR1)-dependent mechanism of metabolism-excitation uncoupling.PMID 18281290Read ↗

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 ↗

Human KATP channelopathies: diseases of metabolic homeostasisSemantic proximity Read ↗

K(ATP) channels and insulin secretion disorders.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 ↗

The Shifting Landscape of K<sub>Atp</sub>Channelopathies and the Need for ‘Sharper’ TherapeuticsSemantic proximity Read ↗

Review. SUR1: a unique ATP-binding cassette protein that functions as an ion channel regulator.Semantic proximity Read ↗

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

Pancreatic β-cell KATP channels: Hypoglycaemia and hyperglycaemia.Semantic proximity Read ↗

ATP-Sensitive Potassium Channels in Hyperinsulinism and Type 2 Diabetes: Inconvenient Paradox or New Paradigm?Semantic proximity Read ↗

Personalized Therapeutics for KATP-Dependent Pathologies.Semantic proximity Read ↗

The Pharmacology of ATP-Sensitive K+ Channels (KATP).Semantic proximity Read ↗

Update of mutations in the genes encoding the pancreatic beta-cell K(ATP) channel subunits Kir6.2 (KCNJ11) and sulfonylurea receptor 1 (ABCC8) in diabetes mellitus and hyperinsulinism.Semantic proximity Read ↗

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