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SIRT4 Inhibits Glutamate Dehydrogenase and Opposes the Effects of Calorie Restriction in Pancreatic β Cells
Sirt3 Mediates Reduction of Oxidative Damage and Prevention of Age-Related Hearing Loss under Caloric Restriction
Mitochondrial DNA Mutations, Oxidative Stress, and Apoptosis in Mammalian Aging
It is shown that mice expressing a proofreading-deficient version of the mitochondrial DNA polymerase g (POLG) accumulate mt DNA mutations and display features of accelerated aging, suggesting that accumulation of mtDNA mutations that promote apoptosis may be a central mechanism driving mammalian aging.
Mitochondrial Fusion Is Required for mtDNA Stability in Skeletal Muscle and Tolerance of mtDNA Mutations
Involvement of mouse Mlh1 in DNA mismatch repair and meiotic crossing over
Findings suggest that Mlh1 is involved in DNA mismatch repair and meiotic crossing over in mice deficient in another mismatch repair gene, M lh1.
Gene-expression profile of the ageing brain in mice
Caloric restriction, which retards the ageing process in mammals, selectively attenuated the age-associated induction of genes encoding inflammatory and stress responses, which resulted in a gene-expression profile indicative of an inflammatory response, oxidative stress and reduced neurotrophic support in both brain regions.
Gene expression profile of aging and its retardation by caloric restriction.
Transcriptional patterns of calorie-restricted animals suggest that caloric restriction retards the aging process by causing a metabolic shift toward increased protein turnover and decreased macromolecular damage.
Calorie restriction and SIRT3 trigger global reprogramming of the mitochondrial protein acetylome.
SIRT1 Redistribution on Chromatin Promotes Genomic Stability but Alters Gene Expression during Aging
Destabilization of tracts of simple repetitive DNA in yeast by mutations affecting DNA mismatch repair
It is shown that mutations in any three yeast genes involved in DNA mismatch repair lead to 100- to 700-fold increases in tract instability, whereas mutations that eliminate the proof-reading function of DNA polymerases have little effect.