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

Single nucleotide polymorphisms in K(ATP) channels: muscular impact on type 2 diabetes.

Diabetes - 1 May 2005

Li Li, Shi Yun, Wang Xueren, Shi Weiwei, Jiang Chun

Abstract excerpt

ATP-sensitive K+ channels (K(ATP) channels) play an important role in glucose homeostasis. A single nucleotide polymorphism (SNP) in the Kir6.2 subunit causes a point mutation of Glu23 to lysine and reduces the ATP sensitivity of pancreatic K(ATP) channels. The SNP found in 58% of Caucasians accounts for 15% of type 2 diabetes. Here we show evidence for dysregulations of muscular K(ATP) channels with the E23K...

Read the complete abstract on PubMed

Topics

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

Share to Amino Acid Substitution
Share to Diabetes Mellitus, Type 2
Share to Membrane Potentials

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Muscle, Skeletal

Share to Obesity

Share to Polymorphism, Single Nucleotide

Share to Potassium Channels, Inwardly Rectifying

Share to Risk Factors

Source

Identifiers

PMID: 15855351
DOI: 10.2337/diabetes.54.5.1592

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

Single nucleotide polymorphisms in K(ATP) channels: muscular impact on type 2 diabetes.PMID 15855351Read ↗

The common single nucleotide polymorphism E23K in K(IR)6.2 sensitizes pancreatic beta-cell ATP-sensitive potassium channels toward activation through nucleoside diphosphates.Semantic proximity Read ↗

Focus on Kir6.2: a key component of the ATP-sensitive potassium channel.Semantic proximity Read ↗

K(IR)6.2 polymorphism predisposes to type 2 diabetes by inducing overactivity of pancreatic beta-cell ATP-sensitive K(+) channels.Semantic proximity Read ↗

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

ATP-dependent potassium channels and type 2 diabetes mellitus.Semantic proximity Read ↗

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

Nucleotide sensitivity of pancreatic ATP-sensitive potassium channels and type 2 diabetes.Semantic proximity Read ↗

Kir6.2 variant E23K increases ATP-sensitive K+ channel activity and is associated with impaired insulin release and enhanced insulin sensitivity in adults with normal glucose tolerance.Semantic proximity Read ↗

The KCNJ11-E23K Gene Variant Hastens Diabetes Progression by Impairing Glucose-Induced Insulin Secretion.Semantic proximity Read ↗

Molecular biology of K(ATP) channels and implications for health and disease.Semantic proximity Read ↗

Kir6.2 polymorphisms sensitize beta-cell ATP-sensitive potassium channels to activation by acyl CoAs: a possible cellular mechanism for increased susceptibility to type 2 diabetes?Semantic proximity Read ↗

The ATP-sensitive K(+) channel ABCC8 S1369A type 2 diabetes risk variant increases MgATPase activity.Semantic proximity Read ↗

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