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• W2148647537 startingPage "1059" @default.
• W2148647537 abstract "ATP-sensitive potassium (K ATP ) channels were first discovered in the heart 30 years ago. Reconstitution of K ATP channel activity by coexpression of members of the pore-forming inward rectifier gene family (Kir6.1, KCNJ8 , and Kir6.2 KCNJ11 ) with sulfonylurea receptors (SUR1, ABCC8 , and SUR2, ABCC9 ) of the ABCC protein subfamily has led to the elucidation of many details of channel gating and pore properties. In addition, the essential roles of Kir6.x and SURx subunits in generating cardiac and vascular K ATP 2 and the detrimental consequences of genetic deletions or mutations in mice have been recognized. However, despite this extensive body of knowledge, there has been a paucity of defined roles of K ATP subunits in human cardiovascular diseases, although there are reports of association of a single Kir6.1 variant with the J-wave syndrome in the ECG, and 2 isolated studies have reported association of loss of function mutations in SUR2 with atrial fibrillation and heart failure. Two new studies convincingly demonstrate that mutations in the SUR2 gene are associated with Cantu syndrome, a complex multi-organ disorder characterized by hypertrichosis, craniofacial dysmorphology, osteochondrodysplasia, patent ductus arteriosus, cardiomegaly, pericardial effusion, and lymphoedema. This realization of previously unconsidered consequences provides significant insight into the roles of the K ATP channel in the cardiovascular system and suggests novel therapeutic possibilities." @default.
• W2148647537 created "2016-06-24" @default.
• W2148647537 creator A5012352667 @default.
• W2148647537 creator A5037494383 @default.
• W2148647537 creator A5088002796 @default.
• W2148647537 date "2013-03-29" @default.
• W2148647537 modified "2023-10-12" @default.
• W2148647537 title "K _ATP Channels and Cardiovascular Disease" @default.
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