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Volumn 277, Issue 21, 2002, Pages 19087-19094

Disabling a C-terminal autoinhibitory control element in endothelial nitric-oxide synthase by phosphorylation provides a molecular explanation for activation of vascular NO synthesis by diverse physiological stimuli

(2) Lane, Paul a,b Gross, Steven S a,b

a Department of Pharmacology ^* (United States)

b WEILL CORNELL MEDICAL COLLEGE (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CALCIUM; ENZYMES; NITROGEN OXIDES; PROTEINS; SYNTHESIS (CHEMICAL);

PHOSPHORYLATION;

BIOCHEMISTRY;

CALMODULIN; ENDOTHELIAL NITRIC OXIDE SYNTHASE; INSULIN; ISOENZYME; NITRIC OXIDE SYNTHASE; SERINE; UNCLASSIFIED DRUG;

ARTICLE; BINDING AFFINITY; CALCIUM CELL LEVEL; CALCIUM TRANSPORT; CARBOXY TERMINAL SEQUENCE; ENZYME PHOSPHORYLATION; INHIBITION KINETICS; MOLECULAR MODEL; NONHUMAN; PHENOTYPE; PRIORITY JOURNAL; PROTEIN BINDING; PROTEIN FUNCTION; SHEAR STRESS; SYNTHESIS; VASCULARIZATION;

AMINO ACID SEQUENCE; ANIMALS; BASE SEQUENCE; CALCIUM; CALMODULIN; CATALYSIS; CATTLE; DNA PRIMERS; ENDOTHELIUM, VASCULAR; MOLECULAR SEQUENCE DATA; MUTAGENESIS, SITE-DIRECTED; NITRIC OXIDE; NITRIC OXIDE SYNTHASE; NITRIC OXIDE SYNTHASE TYPE III; PHOSPHORYLATION; RECOMBINANT PROTEINS; SEQUENCE HOMOLOGY, AMINO ACID;

BOVINAE;

EID: 0037166321 PISSN: 00219258 EISSN: None Source Type: Journal
DOI: 10.1074/jbc.M200258200 Document Type: Article

Times cited : (69)

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