Initiation of Genomic Instability Cellular Senescence and Organismal Aging by Dysfunctional Telomeres

Sandy Chang

Abstract Telomeres are ribonucleoprotein structures that protect the end of linear chromosomes from recognition as DNA double-stranded breaks and activation of a DNA damage response. Telomere-associated proteins also regulate telomerase, the protein responsible for maintaining telomere length. Loss of telomere function results from either alteration in the telosome/shelterin complex that exerts capping function at telomeres, or from progressive loss of telomeric repeats necessary to maintain proper telomeric structure. Dysfunctional telomeres activate p53 to initiate cell cycle arrest/ cellular senescence and may play an important role in aging. Here I describe the use of mouse models to probe the impact of dysfunctional telomeres upon organismal aging.

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