Endothelial Nitric Oxide Synthase Targeting to Caveolae
نویسندگان
چکیده
منابع مشابه
Endothelial nitric oxide synthase targeting to caveolae. Specific interactions with caveolin isoforms in cardiac myocytes and endothelial cells.
The endothelial isoform of nitric oxide synthase (eNOS) modulates cardiac myocyte function and is expressed in the particulate subcellular fraction. We have previously shown that eNOS is targeted to plasmalemmal caveolae in endothelial cells. Caveolae, specialized domains of the plasma membrane, may serve to sequester signaling proteins; a family of transmembrane proteins, the caveolins, form a...
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This review explores advances in our understanding of the intracellular regulation of the endothelial isoform of nitric oxide synthase (eNOS) in the context of its dynamically regulated subcellular targeting. Nitric oxide (NO) is a labile molecule, and may play important biological roles both within the cell in which it is synthesized and in its interactions with nearby cells and molecules. The...
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Caveolin-1, the caveolae scaffolding protein, binds to and negatively regulates eNOS activity. As caveolin-1 also regulates caveolae-mediated endocytosis after activation of the 60-kDa albumin-binding glycoprotein gp60 in endothelial cells, we addressed the possibility that endothelial NO synthase (eNOS)-dependent NO production was functionally coupled to caveolae internalization. We observed t...
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Caveolae, cholesterol rich microdomain platforms localized mostly at the cytoplasmic membrane of endothelial cells as well as other cell types, are importantly involved in cell signaling and enzymatic activity.1–6 Caveolae also contain cationic amino acid transporter (CAT) which provide L-Arginine to the eNOS-Ca -Calmodulin complex toward the production of nitric oxide (NO).1–6 Caveolin-1, a ma...
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Extracellular fluid volume is highly regulated, at least in part, by peripheral resistance and renal function. Nitric oxide (NO) produced by NO synthase type 3 (NOS 3) in the nonrenal vasculature may promote fluid retention by reducing systemic vascular resistance and arterial pressure. In contrast, NO produced by renal NOS 3 promotes water excretion by reducing renal vascular resistance, incre...
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ژورنال
عنوان ژورنال: Journal of Biological Chemistry
سال: 1996
ISSN: 0021-9258
DOI: 10.1074/jbc.271.37.22810