Chromosomal Instability and Aging: Basic Science and - download pdf or read online

By Fuki Hisama, Sherman M. Weissman, George M. Martin

ISBN-10: 0824708563

ISBN-13: 9780824708566

This article examines the connection among DNA harm and service, mobile senescence, genomic instability and ageing. It contains in-depth discussions of varied forms of DNA harm, the DNA fix community, and mobile responses to genetic harm to evaluate their influence at the modulation of getting old approaches and age-related illness, together with melanoma improvement.

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Extra resources for Chromosomal Instability and Aging: Basic Science and Clinical Implications

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2. Threshold Expression Different organs in the human body have different requirements for mitochondrial energy metabolism. It is generally agreed that the brain, heart, and skeletal muscle have the highest energy demands followed by the kidneys, endocrine system, and liver (34). The phenotypic expression of a pathological mtDNA mutation will be determined by the relative proportion of wild-type versus mutant mitochondria in a given tissue. The percentage of mutant mtDNAs needed to impair energy metabolism enough to cause organ dysfunction is called the threshold effect (35).

If neither the p53 nor the pRB pathway is intact, cells may survive with genomic rearrangements and instability, which can lead to cancer and possibly other aging phenotypes. Both apoptosis and cellular senescence suppress tumorigenesis in mammals. However, whereas apoptosis kills and eliminates potential cancer cells, cellular senescence permanently arrests their growth. Recent findings have shed new light on the causes of cellular senescence, the complexity of the senescent phenotype, and the potential consequences of cellular senescence for the development of cancer and aging phenotypes in mammalian organisms.

The effect of donor age on the processing of UV-damaged DNA by cultured human cells: reduced DNA repair capacity and increased DNA mutability. Mutat Res 364:117–123, 1996. D Goukassian, F Gad, M Yaar, MS Eller, US Nehal, BA Gilchrest. Mechanisms and implications of the age-associated decrease in DNA repair capacity. FASEB J 14:1325–1334, 2000. CB Harley, AB Futcher, CW Greider. Telomeres shorten during ageing of human fibroblasts. Nature 345:458–460, 1990. ND Hastie, M Dempster, MG Dunlop, AM Thompson, DK Green, RC Allshire.

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Chromosomal Instability and Aging: Basic Science and Clinical Implications by Fuki Hisama, Sherman M. Weissman, George M. Martin

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Categories: Basic Science