ArticleBiophysical journal2008
DEND mutation in Kir6.2 (KCNJ11) reveals a flexible N-terminal region critical for ATP-sensing of the KATP channel.
Article in Biophysical journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Structural Insights into ATP-Sensitive Potassium Channel Mechanics: A Role of Intrinsically Disordered Regions.Journal of chemical information and modeling · 2023Article
- From glucose sensing to exocytosis: takes from maturity onset diabetes of the young.Frontiers in endocrinology · 2023Review
- New insights into KNature reviews. Endocrinology · 2020Review
- Severe Developmental Delay, Epilepsy and Neonatal Diabetes (DEND) Syndrome: A Case Report.Journal of the ASEAN Federation of Endocrine Societies · 2020Article
- ABCC9/SUR2 in the brain: Implications for hippocampal sclerosis of aging and a potential therapeutic target.Ageing research reviews · 2015Review
- A Conserved Residue Cluster That Governs Kinetics of ATP-dependent Gating of Kir6.2 Potassium Channels.The Journal of biological chemistry · 2015Article
- Systemic Administration of Glibenclamide Fails to Achieve Therapeutic Levels in the Brain and Cerebrospinal Fluid of Rodents.PloS one · 2015Article
- Decomposition of slide helix contributions to ATP-dependent inhibition of Kir6.2 channels.The Journal of biological chemistry · 2013Article
- Article
- Engineered interaction between SUR1 and Kir6.2 that enhances ATP sensitivity in KATP channels.The Journal of general physiology · 2012Article
- Channeling dysglycemia: ion-channel variations perturbing glucose homeostasis.Trends in endocrinology and metabolism: TEM · 2012Review
- Hydrogen sulfide as endothelium-derived hyperpolarizing factor sulfhydrates potassium channels.Circulation research · 2011Article
- The molecular mechanisms and pharmacotherapy of ATP-sensitive potassium channel gene mutations underlying neonatal diabetes.Pharmacogenomics and personalized medicine · 2010Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
ATP-sensitive K(+)-channels link metabolism and excitability in neurons, myocytes, and pancreatic islets. Mutations in the pore-forming subunit (Kir6.2; KCNJ11) cause neonatal diabetes, developmental delay, and epilepsy by decreasing sensitivity to ATP inhibition and suppressing electrical activity. Mutations of residue G53 underlie both mild (G53R,S) and severe (G53D) forms of the disease. All examined substitutions (G53D,R,S,A,C,F) reduced ATP-sensitivity, indicating an intolerance of any amino acid other than glycine. Surprisingly, each mutation reduces ATP affinity, rather than intrinsic gating, although structural modeling places G53 at a significant distance from the ATP-binding pocket. We propose that glycine is required in this location for flexibility of the distal N-terminus, and for an induced fit of ATP at the binding site. Consistent with this hypothesis, glycine substitution of the adjacent residue (Q52G) partially rescues ATP affinity of reconstituted Q52G/G53D channels. The results reveal an important feature of the noncanonical ATP-sensing mechanism of K(ATP) channels.
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