ArticleThe Journal of physiology2006
Functional effects of naturally occurring KCNJ11 mutations causing neonatal diabetes on cloned cardiac KATP channels.
Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 37 citations in OpenAlex.
- Dynamic duo: Kir6 and SUR in KChannels (Austin, Tex.) · 2024Review
- Structure of an open KNature communications · 2024Article
- Personalized Therapeutics for KAnnual review of pharmacology and toxicology · 2023Review
- From glucose sensing to exocytosis: takes from maturity onset diabetes of the young.Frontiers in endocrinology · 2023Review
- Development of IFrontiers in pharmacology · 2021Article
- New insights into KNature reviews. Endocrinology · 2020Review
- Sensitivity of KATP channels to cellular metabolic disorders and the underlying structural basis.Acta pharmacologica Sinica · 2016Article
- Switching to sulphonylureas in children with iDEND syndrome caused by KCNJ11 mutations results in improved cerebellar perfusion.Diabetes care · 2013Article
- Engineered interaction between SUR1 and Kir6.2 that enhances ATP sensitivity in KATP channels.The Journal of general physiology · 2012Article
- Ankyrin-B regulates Kir6.2 membrane expression and function in heart.The Journal of biological chemistry · 2010Article
- K(ATP) channelopathies in the pancreas.Pflugers Archiv : European journal of physiology · 2010Review
- Dual role of K ATP channel C-terminal motif in membrane targeting and metabolic regulation.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- An in-frame deletion in Kir6.2 (KCNJ11) causing neonatal diabetes reveals a site of interaction between Kir6.2 and SUR1.The Journal of clinical endocrinology and metabolism · 2009Article
- Secondary consequences of beta cell inexcitability: identification and prevention in a murine model of K(ATP)-induced neonatal diabetes mellitus.Cell metabolism · 2009Article
- Review. SUR1: a unique ATP-binding cassette protein that functions as an ion channel regulator.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2009Review
- Neonatal diabetes mellitus.Endocrine reviews · 2008Review
- The Kir6.2-F333I mutation differentially modulates KATP channels composed of SUR1 or SUR2 subunits.The Journal of physiology · 2007Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
ATP-sensitive K+ (K(ATP)) channels are hetero-octamers of inwardly rectifying K+ channel (Kir6.2) and sulphonylurea receptor subunits (SUR1 in pancreatic beta-cells, SUR2A in heart). Heterozygous gain-of-function mutations in Kir6.2 cause neonatal diabetes, which may be accompanied by epilepsy and developmental delay. However, despite the importance of K(ATP) channels in the heart, patients have no obvious cardiac problems. We examined the effects of adenine nucleotides on K(ATP) channels containing wild-type or mutant (Q52R, R201H) Kir6.2 plus either SUR1 or SUR2A. In the absence of Mg2+, both mutations reduced ATP inhibition of SUR1- and SUR2A-containing channels to similar extents, but when Mg2+ was present ATP blocked mutant channels containing SUR1 much less than SUR2A channels. Mg-nucleotide activation of SUR1, but not SUR2A, channels was markedly increased by the R201H mutation. Both mutations also increased resting whole-cell K(ATP) currents through heterozygous SUR1-containing channels to a greater extent than for heterozygous SUR2A-containing channels. The greater ATP inhibition of mutant Kir6.2/SUR2A than of Kir6.2/SUR1 can explain why gain-of-function Kir6.2 mutations manifest effects in brain and beta-cells but not in the heart.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.