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

Hyperinsulinism-Causing Mutations Cause Multiple Molecular Defects in SUR1 NBD1.

Biochemistry - 9 May 2017

Alvarez Claudia P, Stagljar Marijana, Muhandiram D Ranjith, Kanelis Voula

Abstract excerpt

The sulfonylurea receptor 1 (SUR1) protein forms the regulatory subunit in ATP sensitive K+ (KATP) channels in the pancreas. SUR proteins are members of the ATP binding cassette (ABC) superfamily of proteins. Binding and hydrolysis of MgATP at the SUR nucleotide binding domains (NBDs) lead to channel opening. Pancreatic KATP channels play an important role in insulin secretion. SUR1 mutations that result in...

Read the complete abstract on PubMed

Topics

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

Share to Hyperinsulinism
Share to Lysine
Share to Pancreas

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Protein Aggregates

Share to Protein Conformation, alpha-Helical

Share to Protein Interaction Domains and Motifs

Share to Sulfonylurea Receptors

Share to Threonine

Source

Identifiers

PMID: 28346775
DOI: 10.1021/acs.biochem.6b00681

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Hyperinsulinism-Causing Mutations Cause Multiple Molecular Defects in SUR1 NBD1.PMID 28346775Read ↗

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

Dominantly inherited hyperinsulinism caused by a mutation in the sulfonylurea receptor type 1Semantic proximity Read ↗

A mutation (R826W) in nucleotide-binding domain 1 of ABCC8 reduces ATPase activity and causes transient neonatal diabetes.Semantic proximity Read ↗

Functional analyses of novel mutations in the sulfonylurea receptor 1 associated with persistent hyperinsulinemic hypoglycemia of infancy.Semantic proximity Read ↗

Mutations of the same conserved glutamate residue in NBD2 of the sulfonylurea receptor 1 subunit of the KATP channel can result in either hyperinsulinism or neonatal diabetes.Semantic proximity Read ↗

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

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

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

Sulfonylurea receptor 1 mutations that cause opposite insulin secretion defects with chemical chaperone exposure.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 heterozygous activating mutation in the sulphonylurea receptor SUR1 (ABCC8) causes neonatal diabetes.Semantic proximity Read ↗

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