Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik

Permanent URI for this collectionhttps://hdl.handle.net/11147/9

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Publisher: search.filters.publisher.John Wiley and Sons Inc.Subject: search.filters.subject.Aging

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  • Article
    Citation - WoS: 29
    Citation - Scopus: 29
    Methionine Sulfoxide Reduction and the Aging Process
    (John Wiley and Sons Inc., 2007) Koç, Ahmet; Gladyshev, Vadim N.
    Aging has been described for multicellular and asymmetrically dividing organisms, but the mechanisms are poorly understood. Oxidation of proteins is considered to be one of the major factors that leads to aging. Oxidative damage to proteins results in the oxidation of certain amino acid residues, among which oxidation of sulfur-containing amino acids, methionine and cysteine, is notable because of the susceptibility of these residues to damage, and occurrence of repair mechanisms. Methionine sulfoxide reductases, MsrA and MsrB, are thioredoxin-dependent oxidoreductases that reduce oxidized forms of methionine, methionine sulfoxides, in a stereospecific manner. These enzymes are present in all cell types and have shown to be regulating life spans in mammals, insects, and yeast. Here, their roles in modulating yeast life span are discussed.
  • Article
    Citation - WoS: 59
    Citation - Scopus: 60
    Effects of Deleting Mitochondrial Antioxidant Genes on Life Span
    (John Wiley and Sons Inc., 2007) Ünlü, Ercan Selçuk; Koç, Ahmet
    Reactive oxygen species (ROS) damage biomolecules, accelerate aging, and shorten life span, whereas antioxidant enzymes mitigate these effects. Because mitochondria are a primary site of ROS generation and also a primary target of ROS attack, they have become a major focus area of aging studies. Here, we employed yeast genetics to identify mitochondrial antioxidant genes that are important for replicative life span. In our studies, it was found that among the known mitochondrial antioxidant genes (TTR1, CCD1, SOD1, GLO4, TRR2, TRX3, CCS1, SOD2, GRX5, PRX1), deletion of only three genes, SOD1 (Cu, Zn superoxide dismutase), SOD2 (Manganese-containing superoxide dismutase), and CCS1 (Copper chaperone), shortened the life span enormously. The life span decreased 40% for Δsod1 mutant, 72% for Δsod2 mutant, and 50% for Δccs1 mutant. Deletion of the other genes had little or no effect on life span.