期刊
MEMORIAS DO INSTITUTO OSWALDO CRUZ
卷 100, 期 -, 页码 15-18出版社
FUNDACO OSWALDO CRUZ
DOI: 10.1590/S0074-02762005000900004
关键词
nitric oxide; endothelium; caveolin-1; heat shock protein 90; atherosclerosis; inflammation
Endothelial nitric oxide synthase (eNOS) is the primary physiological source of nitric oxide (NO) that regulates cardiovascular homeostasis. Historically eNOS has been thought to be a constitutively expressed enzyme regulated by calcium and calmodulin. However in the last five years it is clear that eNOS activity and NO release can be regulated by post-translational control mechanisms (fatty acid modification and phosphorylation) and protein-protein interactions (with caveolin-1 and heat shock protein 90) that direct impinge upon the duration and magnitude of NO release. This review will summarize this information and apply the post-translational control mechanisms to disease states.
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