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TRIB3 R84 Variant Is Associated With Impaired Insulin-Mediated Nitric Oxide Production in Human Endothelial Cells
Author(s) -
Francesco Andreozzi,
Gloria Formoso,
Sabrina Prudente,
Marta Letizia Hribal,
Assunta Pandolfi,
Emanuele Bellacchio,
Sara Di Silvestre,
Vincenzo Trischitta,
Agostino Consoli,
Giorgio Sesti
Publication year - 2008
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.108.162883
Subject(s) - protein kinase b , insulin , enos , medicine , nitric oxide , insulin receptor , umbilical vein , endocrinology , insulin resistance , biology , endothelium , phosphorylation , microbiology and biotechnology , nitric oxide synthase , biochemistry , in vitro
In the endothelium, insulin promotes nitric oxide (NO) production, through the insulin receptor/IRS-1/PI3-Kinase/Akt/eNOS signaling pathway. An inhibitor of insulin action, TRIB3, has recently been identified which affects insulin action by binding to and inhibiting Akt phosphorylation. We have recently described a Q84R gain-of-function polymorphism of TRIB3 with the R84 variant being associated with insulin resistance and an earlier age at myocardial infarction.

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