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

The Kir6.2-F333I mutation differentially modulates KATP channels composed of SUR1 or SUR2 subunits.

The Journal of physiology - 15 Jun 2007

Tammaro Paolo, Ashcroft Frances

Abstract excerpt

Mutations in Kir6.2, the pore-forming subunit of the KATP channel, that reduce the ability of ATP to block the channel cause neonatal diabetes. The stimulatory effect of MgATP mediated by the regulatory sulphonylurea receptor (SUR) subunit of the channel may also be modified. We compared the effect of the Kir6.2-F333I mutation on KATP channels containing SUR1, SUR2A or SUR2B. The open probability of Kir6.2/SUR1...

Read the complete abstract on PubMed

Topics

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

Share to Adenosine Diphosphate
Share to Guanosine Diphosphate
Share to Magnesium

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Multidrug Resistance-Associated Proteins

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: 17395632
DOI: 10.1113/jphysiol.2007.130211
PMCID: PMC1976406

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. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The Kir6.2-F333I mutation differentially modulates KATP channels composed of SUR1 or SUR2 subunits.PMID 17395632Read ↗

Kir6.2 mutations causing neonatal diabetes provide new insights into Kir6.2-SUR1 interactions.Semantic proximity Read ↗

A mutation in the ATP-binding site of the Kir6.2 subunit of the KATP channel alters coupling with the SUR2A subunit.Semantic proximity Read ↗

Adjacent mutations in the gating loop of Kir6.2 produce neonatal diabetes and hyperinsulinismSemantic proximity Read ↗

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

Functional effects of naturally occurring KCNJ11 mutations causing neonatal diabetes on cloned cardiac KATP channels.Semantic proximity Read ↗

Functional effects of KCNJ11 mutations causing neonatal diabetes: enhanced activation by MgATP.Semantic proximity Read ↗

Neonatal diabetes caused by mutations in sulfonylurea receptor 1: interplay between expression and Mg-nucleotide gating defects of ATP-sensitive potassium channels.Semantic proximity Read ↗

Functional effects of mutations at F35 in the NH2-terminus of Kir6.2 (KCNJ11), causing neonatal diabetes, and response to sulfonylurea therapy.Semantic proximity Read ↗

Molecular determinants of KATP channel inhibition by ATP.Semantic proximity Read ↗

Three C-terminal residues from the sulphonylurea receptor contribute to the functional coupling between the K(ATP) channel subunits SUR2A and Kir6.2.Semantic proximity Read ↗

Mechanism of action of a sulphonylurea receptor SUR1 mutation (F132L) that causes DEND syndrome.Semantic proximity Read ↗

MgATP activates the beta cell KATP channel by interaction with its SUR1 subunit.Semantic proximity Read ↗

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