The oncogenic RAS2val19 mutation locks respiration, independently of PKA, in a mode prone to generate ROS

EMBO Journal

Volumn 22, Issue 13, 2003, Pages 3337-3345

  Hlavatá, Lydie ^a   Aguilaniu, Hugo ^b   Pichová, Alena ^a   Nyström, Thomas ^b  

^a INSTITUTE OF MICROBIOLOGY   (Czech Republic)

^b UNIVERSITY OF GOTHENBURG   (Sweden)

Author keywords

PKA; RAS2; Reactive oxygen species; Replicative aging; Respiratory state; UCP1

Indexed keywords

CYCLIC AMP DEPENDENT PROTEIN KINASE; MUTANT PROTEIN; RAS PROTEIN; REACTIVE OXYGEN METABOLITE; UNCOUPLING PROTEIN 1;

ALLELE; ARTICLE; CELL AGING; CELL DIVISION; CONTROLLED STUDY; GENE MUTATION; GENE STRUCTURE; MITOCHONDRIAL RESPIRATION; NONHUMAN; ONCOGENE RAS; OXIDATION; OXIDATIVE STRESS; PHENOTYPE; PRIORITY JOURNAL; PROTEIN DEFECT; PROTEIN PHOSPHORYLATION; SIGNAL TRANSDUCTION; STRESS RESPONSE ELEMENT; YEAST;

ALLELES; CYCLIC AMP; CYCLIC AMP-DEPENDENT PROTEIN KINASES; MUTATION; ONCOGENE PROTEIN P21(RAS); OXIDATIVE STRESS; PHOSPHORYLATION; REACTIVE OXYGEN SPECIES; SACCHAROMYCES CEREVISIAE; VALINE;

MAMMALIA;

EID: 0038263852     PISSN: 02614189     EISSN: None     Source Type: Journal    
DOI: 10.1093/emboj/cdg314     Document Type: Article

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