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A gating mutation at the internal mouth of the Kir6.2 pore is associated with DEND syndrome.Kir6.2 孔道内口处的门控突变与 DEND 综合征相关。
EMBO Rep. 2005 May;6(5):470-5. doi: 10.1038/sj.embor.7400393.
2
The C42R mutation in the Kir6.2 (KCNJ11) gene as a cause of transient neonatal diabetes, childhood diabetes, or later-onset, apparently type 2 diabetes mellitus.Kir6.2（KCNJ11）基因中的C42R突变是导致短暂性新生儿糖尿病、儿童糖尿病或迟发性2型糖尿病的原因。
J Clin Endocrinol Metab. 2005 Jun;90(6):3174-8. doi: 10.1210/jc.2005-0096. Epub 2005 Mar 22.
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Relapsing diabetes can result from moderately activating mutations in KCNJ11.复发性糖尿病可能由KCNJ11基因中的中度激活突变引起。
Hum Mol Genet. 2005 Apr 1;14(7):925-34. doi: 10.1093/hmg/ddi086. Epub 2005 Feb 17.
4
Functional analysis of a structural model of the ATP-binding site of the KATP channel Kir6.2 subunit.KATP通道Kir6.2亚基ATP结合位点结构模型的功能分析
EMBO J. 2005 Jan 26;24(2):229-39. doi: 10.1038/sj.emboj.7600487. Epub 2005 Jan 13.
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Molecular basis of Kir6.2 mutations associated with neonatal diabetes or neonatal diabetes plus neurological features.与新生儿糖尿病或伴有神经学特征的新生儿糖尿病相关的Kir6.2突变的分子基础。
Proc Natl Acad Sci U S A. 2004 Dec 14;101(50):17539-44. doi: 10.1073/pnas.0404756101. Epub 2004 Dec 6.
6
KCNJ11 activating mutations in Italian patients with permanent neonatal diabetes.意大利永久性新生儿糖尿病患者中的KCNJ11激活突变
Hum Mutat. 2005 Jan;25(1):22-7. doi: 10.1002/humu.20124.
7
Genotype-phenotype correlations in children with congenital hyperinsulinism due to recessive mutations of the adenosine triphosphate-sensitive potassium channel genes.因三磷酸腺苷敏感性钾通道基因隐性突变所致先天性高胰岛素血症患儿的基因型-表型相关性
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Identification of a functionally important negatively charged residue within the second catalytic site of the SUR1 nucleotide-binding domains.在SUR1核苷酸结合结构域的第二个催化位点内鉴定出一个功能重要的带负电荷残基。
Diabetes. 2004 Dec;53 Suppl 3:S123-7. doi: 10.2337/diabetes.53.suppl_3.s123.
9
Glibenclamide treatment in permanent neonatal diabetes mellitus due to an activating mutation in Kir6.2.由于Kir6.2激活突变导致的永久性新生儿糖尿病中的格列本脲治疗。
J Clin Endocrinol Metab. 2004 Nov;89(11):5504-7. doi: 10.1210/jc.2004-1241.
10
Common variants of the hepatocyte nuclear factor-4alpha P2 promoter are associated with type 2 diabetes in the U.K. population.肝细胞核因子-4α P2启动子的常见变异与英国人群中的2型糖尿病相关。
Diabetes. 2004 Nov;53(11):3002-6. doi: 10.2337/diabetes.53.11.3002.

ATP敏感性钾通道病：聚焦于胰岛素分泌

ATP-sensitive potassium channelopathies: focus on insulin secretion.

作者信息

Ashcroft Frances M

机构信息

University Laboratory of Physiology, Oxford University, Oxford, United Kingdom.

出版信息

J Clin Invest. 2005 Aug;115(8):2047-58. doi: 10.1172/JCI25495.

DOI:10.1172/JCI25495
PMID:16075046
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1180549/
Abstract

ATP-sensitive potassium (K(ATP)) channels, so named because they are inhibited by intracellular (ATP), play key physiological roles in many tissues. In pancreatic beta cells, these channels regulate glucose-dependent insulin secretion and serve as the target for sulfonylurea drugs used to treat type 2 diabetes. This review focuses on insulin secretory disorders, such as congenital hyperinsulinemia and neonatal diabetes, that result from mutations in K(ATP) channel genes. It also considers the extent to which defective regulation of K(ATP) channel activity contributes to the etiology of type 2 diabetes.

摘要

ATP敏感性钾（K(ATP)）通道，因其受细胞内ATP抑制而得名，在许多组织中发挥关键的生理作用。在胰腺β细胞中，这些通道调节葡萄糖依赖性胰岛素分泌，并作为用于治疗2型糖尿病的磺脲类药物的靶点。本综述聚焦于由K(ATP)通道基因突变导致的胰岛素分泌紊乱，如先天性高胰岛素血症和新生儿糖尿病。它还探讨了K(ATP)通道活性调节缺陷在2型糖尿病病因学中的作用程度。