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机构地区:[1]江苏省心血管病分子干预重点实验室,南京医科大学动脉粥样硬化研究中心,南京210029
出 处:《转化医学研究(电子版)》2013年第4期18-35,共18页Translational Medicine Research(Electronic Edition)
摘 要:内皮型一氧化氮合酶(endothelial nitric oxide synthase,eNOS)翻译后调节机制复杂,可直接通过磷酸化、乙酰化等多种形式的修饰改变活性,同时钙调蛋白、小凹蛋白、热休克蛋白90、G蛋白偶联受体、激酶、骨架蛋白等多种蛋白质可通过与eNOS直接或间接作用,调节eNOS的活性;BH4和吡哆醇可通过影响脱偶联调控eNOS的活性。对eNOS调节机制的探讨将有利于发现防治内皮功能障碍相关疾病的新靶点。The post-translational regulatory mechanism of endothelial nitric oxide synthase( eNOS) is a complicated process concerning the regulation of its activity with multiple modifications,including phosphorylation,acetylation etc. Various proteins,such as calmodulin,caveolin,heat shock protein 90,G protein-coupled receptors,kinases and cytoskeletal proteins showed direct or indirect interactions with eNOS to regulate its activity. In addition,BH4 and pyridoxine can also regulate the eNOS activity through eNOS uncoupling pathway. Studies about regulatory mechanism of eNOS would help us to find novel targets in prevention and treatment of endothelial dysfunctions related to various diseases.
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