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免疫病理疾病及治疗学论文学
SJR: 0.309 SNIP: 0.041 CiteScore™: 0.18

ISSN 打印: 2151-8017
ISSN 在线: 2151-8025

Archives: Volume 1, 2010 to Volume 7, 2016

免疫病理疾病及治疗学论文学

DOI: 10.1615/ForumImmunDisTher.2012006133
pages 135-139

Ras Denitrosylation in Human Lung Cancer

Benjamin Gaston
University of Virginia School of Medicine, Department of Pediatrics, Charlottesville, Virginia
Nadzeya Marozkina
University of Virginia School of Medicine, Department of Pediatrics, Charlottesville, Virginia

ABSTRACT

S-nitrosylation and denitrosylation are regulated signaling reactions. They are also relevant to the toxicology of nitrogen oxides. S-nitrosoglutathione (GSNO) reductase is an important denitrosylating enzyme, acting through intermediate GSNO formation from S-nitrosylated proteins and from reduced glutathione. It also serves to protect cells from excessive nitrosative stress. Endothelial nitric oxide synthase (NOS) activation downstream of oncogenic Ras causes S-nitrosylation of wild-type Ras that is necessary for oncogenesis. GSNO reductase serves as a Ras denitrosylase, protecting against oncogenesis. Exposure to exogenous nitric oxide, such as that present in high concentrations in cigarette smoke, also S-nitrosylates Ras. GSNO reductase expression and activity are decreased in various types of lung cancer. Taken together, these data suggest that GSNO reductase expression is important for protection against the tumorigenic effects, mediated by Ras S-nitrosylation, of both overactivation of endothelial NOS and chronic exposure to smoke.


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