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Many life span influencing genes affect the rate of DNA damage or DNA repair. Genetics of aging is generally concerned with life extension associated with genetic alterations, rather than with accelerated aging diseases leading to reduction in lifespan. The first mutation found to increase longevity in an animal was the age-1 gene in ...
Most of the DNA repair deficiency diseases show varying degrees of "accelerated aging" or cancer (often some of both). [37] But elimination of any gene essential for base excision repair kills the embryo—it is too lethal to display symptoms (much less symptoms of cancer or "accelerated aging"). [38]
Lamin proteins are thought to be involved in nuclear stability, chromatin structure and gene expression. Vertebrate lamins consist of two types, A and B. Through alternate splicing, this gene encodes three type A lamin isoforms. [10]
In cultured human neurons, these gene promoters are selectively damaged by oxidative stress. Thus Lu et al. [36] concluded that DNA damage may reduce the expression of selectively vulnerable genes involved in learning, memory and neuronal survival, initiating a program of brain aging that starts early in adult life. [citation needed]
DAF-16 is the sole ortholog of the FOXO family of transcription factors in the nematode Caenorhabditis elegans. [1] It is responsible for activating genes involved in longevity, lipogenesis, heat shock survival and oxidative stress responses.
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The Rb tumor suppressor has been shown to associate with E2F1 (a protein necessary for transcription) in its monophosphorylated form, which inhibits transcription of downstream target genes involved in the G1/S transition. [44] As part of a feedback loop, increased phosphorylation of Rb increases p16 expression that inhibits Cdk4/6.
The mutation accumulation theory of aging was first proposed by Peter Medawar in 1952 as an evolutionary explanation for biological aging and the associated decline in fitness that accompanies it. [1] Medawar used the term 'senescence' to refer to this process.