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

Identification of mutations in the Kir6.2 subunit of the K(ATP) channel.

Methods in molecular biology (Clifton, N.J.) - 1 Jan 2008

Flanagan Sarah E, Ellard Sian

Abstract excerpt

The beta-cell ATP-sensitive potassium channel is a key component of stimulus -secretion coupling in the pancreatic beta-cell. The channel consists of four subunits of the inwardly rectifying potassium channel Kir6.2 and four subunits of the sulfonylurea receptor 1. Loss of function mutations in the KCNJ11 and ABCC8 genes that encode for Kir6.2 and SUR1 can cause over-secretion of insulin and result in...

Read the complete abstract on PubMed

Topics

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

Share to Diabetes Mellitus
Share to DNA Primers
Share to Gene Amplification

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Infant, Newborn

Share to KATP Channels

Share to Leukocytes

Share to Potassium Channels, Inwardly Rectifying

Share to Protein Subunits

Source

Identifiers

PMID: 18998097
DOI: 10.1007/978-1-59745-526-8_18

Genes

KCNJ11
ABCC8

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Identification of mutations in the Kir6.2 subunit of the K(ATP) channel.PMID 18998097Read ↗

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 ↗

Mutations in the genes encoding the pancreatic beta-cell KATP channel subunits Kir6.2 (KCNJ11) and SUR1 (ABCC8) in diabetes mellitus and hyperinsulinism.Semantic proximity Read ↗

A loss-of-function mutation in KCNJ11 causing sulfonylurea-sensitive diabetes in early adult life.Semantic proximity Read ↗

Update of variants identified in the pancreatic β-cell KATP channel genes KCNJ11 and ABCC8 in individuals with congenital hyperinsulinism and diabetes.Semantic proximity Read ↗

Diabetes and hypoglycaemia in young children and mutations in the Kir6.2 subunit of the potassium channel: therapeutic consequences.Semantic proximity Read ↗

New insights into KATP channel gene mutations and neonatal diabetes mellitus.Semantic proximity Read ↗

Functional analysis of six Kir6.2 (KCNJ11) mutations causing neonatal diabetes.Semantic proximity Read ↗

Methods for Characterizing Disease-Associated ATP-Sensitive Potassium Channel Mutations.Semantic proximity Read ↗

Mutation of the pancreatic islet inward rectifier Kir6.2 also leads to familial persistent hyperinsulinemic hypoglycemia of infancy.Semantic proximity Read ↗

Activating mutations in Kir6.2 and neonatal diabetes: new clinical syndromes, new scientific insights, and new therapy.Semantic proximity Read ↗

Mutations in the Kir6.2 subunit of the KATP channel and permanent neonatal diabetes: new insights and new treatment.Semantic proximity Read ↗

Neonatal diabetes: an expanding list of genes allows for improved diagnosis and treatment.Semantic proximity Read ↗

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