Glutaredoxin mediates Akt and eNOS activation by flow in a glutathione reductase-dependent manner

Arteriosclerosis, Thrombosis, and Vascular Biology

Volumn 27, Issue 6, 2007, Pages 1283-1288

  Wang, Jing ^a   Pan, Shi ^a   Berk, Bradford C ^a  

^a UNIVERSITY OF ROCHESTER MEDICAL CENTER   (United States)

Author keywords

Akt; Endothelial cells; eNOS; GR; Grx

Indexed keywords

CARMUSTINE; ENDOTHELIAL NITRIC OXIDE SYNTHASE; ENZYME; GLUTAREDOXIN; GLUTATHIONE; GLUTATHIONE REDUCTASE; PROTEIN KINASE B; SMALL INTERFERING RNA; THIOLTRANSFERASE; UNCLASSIFIED DRUG;

ANIMAL CELL; ARTICLE; CONTROLLED STUDY; COW; ENDOTHELIUM CELL; ENZYME ACTIVATION; ENZYME ACTIVITY; GENE OVEREXPRESSION; HUMAN; HUMAN CELL; LAMINAR FLOW; NONHUMAN; PHOSPHORYLATION; PRIORITY JOURNAL; SHEAR STRESS; STATISTICAL SIGNIFICANCE; UMBILICAL VEIN;

ANIMALS; CARMUSTINE; CATTLE; CELLS, CULTURED; ENDOTHELIAL CELLS; ENVIRONMENT, CONTROLLED; ENZYME ACTIVATION; ENZYME INHIBITORS; GLUTATHIONE; GLUTATHIONE REDUCTASE; HUMANS; MUTATION; NITRIC OXIDE SYNTHASE TYPE III; OXIDATION-REDUCTION; OXIDOREDUCTASES; PHOSPHORYLATION; PROTO-ONCOGENE PROTEINS C-AKT; RNA INTERFERENCE; RNA, SMALL INTERFERING; SIGNAL TRANSDUCTION; STRESS, MECHANICAL; TRANSFECTION;

EID: 34249309215     PISSN: 10795642     EISSN: None     Source Type: Journal    
DOI: 10.1161/ATVBAHA.107.144659     Document Type: Article

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