Regulation of HERG proteins by chemical chaperones

化学伴侣对 HERG 蛋白的调节

• 批准号: 6619673
• 负责人: Brian P Delisle
• 金额: $ 4.64万
• 依托单位: UNIVERSITY OF WISCONSIN-MADISON
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-08-01 至 2005-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6619673
• 关键词: antiarrhythmic agent; antihistamines; cisapride; glycosylation; heart pharmacology; long QT syndrome; membrane activity; molecular chaperones; postdoctoral investigator; potassium channel; protein transport; tissue /cell culture; western blottings

DESCRIPTION (provided by applicant): The long-term goal of this project is to investigate the pharmacological rescue of ion channels that fail to traffic normally to the plasma membrane. Failure of protein trafficking underlies ion channelopathies associated with congenital Long QT2 syndrome (LQT2). Drugs that bind to channels with a high affinity can restore the trafficking defects of mutant ion channels. However, the mechanisms that underlie the drug rescue of these channels remain poorly understood. This proposal examines the differences in pharmacological rescue of Long QT2 trafficking defects at the molecular and functional level.

描述（由申请人提供）：该项目的长期目标是调查未能正常运输到质膜的离子通道的药理营救。蛋白运输的失败是与先天长QT2综合征相关的离子通道病（LQT2）。与具有高亲和力的通道结合的药物可以恢复突变离子通道的运输缺陷。但是，这些通道的药物营救基础的机制仍然鲜为人知。该提案研究了分子和功能水平上长QT2运输缺陷的药理营救的差异。