1.
Mem. Inst. Oswaldo Cruz
;
100(supl.1): 15-18, Mar. 2005.
Article
in English
| LILACS
| ID: lil-402170
ABSTRACT
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.
Subject(s)
Animals , Humans , Arteriosclerosis/metabolism , Diabetes Mellitus/metabolism , Endothelium, Vascular/metabolism , Liver Cirrhosis/metabolism , Nitric Oxide Synthase Type III/metabolism , Nitric Oxide/metabolism , Caveolin 1/physiology , Enzyme Activation , HSP90 Heat-Shock Proteins/physiology
2.
Rev. argent. mastología
;
13(39): 32-43, abr. 1994. tab, graf
Article
in Spanish
| LILACS
| ID: lil-184618