ArticleDiabetes & metabolism journal2013
Neonatal diabetes caused by activating mutations in the sulphonylurea receptor.
Article in Diabetes & metabolism journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Clinical and Genetic Characteristics ofJournal of diabetes research · 2021Pooled it
- Structure based analysis of KScientific reports · 2021Article
- Long-term Follow-up of Glycemic and Neurological Outcomes in an International Series of Patients With Sulfonylurea-TreatedDiabetes care · 2021Article
- Cantu syndrome-associated SUR2 (ABCC9) mutations in distinct structural domains result in KThe Journal of biological chemistry · 2018Article
- KInternal medicine (Tokyo, Japan) · 2017Review
- Molecular action of sulphonylureas on KATP channels: a real partnership between drugs and nucleotides.Biochemical Society transactions · 2015Review
Corrections and comments
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Authors and funding
1 author.
Funding
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Abstract
Adenosine triphosphate (ATP)-sensitive potassium (KATP) channels in pancreatic β-cells play a crucial role in insulin secretion and glucose homeostasis. These channels are composed of two subunits: a pore-forming subunit (Kir6.2) and a regulatory subunit (sulphonylurea receptor-1). Recent studies identified large number of gain of function mutations in the regulatory subunit of the channel which cause neonatal diabetes. Majority of mutations cause neonatal diabetes alone, however some lead to a severe form of neonatal diabetes with associated neurological complications. This review focuses on the functional effects of these mutations as well as the implications for treatment.
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