1.
Mem. Inst. Oswaldo Cruz
;
100(supl.1): 15-18, Mar. 2005.
Artigo
em Inglês
| LILACS
| ID: lil-402170
RESUMO
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.
Assuntos
Animais , Humanos , Arteriosclerose/metabolismo , Diabetes Mellitus/metabolismo , Endotélio Vascular/metabolismo , Cirrose Hepática/metabolismo , Óxido Nítrico Sintase Tipo III/metabolismo , Óxido Nítrico/metabolismo , Caveolina 1/fisiologia , Ativação Enzimática , Proteínas de Choque Térmico HSP90/fisiologia
2.
Rev. argent. mastología
;
13(39): 32-43, abr. 1994. tab, graf
Artigo
em Espanhol
| LILACS
| ID: lil-184618