By Fuki Hisama, Sherman M. Weissman, George M. Martin
This article examines the connection among DNA harm and service, mobile senescence, genomic instability and getting old. It contains in-depth discussions of assorted different types of DNA harm, the DNA fix community, and mobile responses to genetic harm to evaluate their impression at the modulation of getting older techniques and age-related affliction, together with melanoma improvement.
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Additional info for Chromosomal Instability and Aging: Basic Science and Clinical Implications
DNA damage triggers a prolonged p53-dependent G1 arrest and long-term induction of Cip1 in normal human fibroblasts. Genes Dev 8:2540–2551, 1994. Q Chen, A Fischer, JD Reagan, LJ Yan, BN Ames. Oxidative DNA damage and senescence of human diploid fibroblast cells. Proc Natl Acad Sci USA 92:4337– 4341, 1995. VV Ogryzko, TH Hirai, VR Russanova, DA Barbie, BH Howard. Human fibroblast commitment to a senescence-like state in response to histone deacetylase inhibitors is cell cycle dependent. Mol Cell Biol 16:5210–5218, 1996.
The p53 protein is a transcriptional activator and repressor whose activity is regulated primarily by the balance between synthesis and degradation and by posttranslational modifications such as phosphorylation and acetylation. It controls the expression of numerous genes, many of which cause transient cell cycle arrest, cellular senescence, or apoptosis in response to DNA damage and other stimuli. One of these genes encodes the p21 CDKI that is highly expressed by senescent cells (105,133,134).
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Chromosomal Instability and Aging: Basic Science and Clinical Implications by Fuki Hisama, Sherman M. Weissman, George M. Martin