ePrints

Telomeres and replicative senescence: Is it only length that counts?

Lookup NU author(s): Professor Thomas von Zglinicki

Downloads

Full text for this publication is not currently held within this repository. Alternative links are provided below where available.

Abstract

Telomeres are well established as a major 'replicometer', counting the population doublings in primary human cell cultures and ultimately triggering replicative senescence. However, neither is the pace of this biological clock inert, nor is there a fixed threshold telomere length acting as the universal trigger of replicative senescence. The available data suggest that opening of the telomeric loop and unscheduled exposure of the single-stranded G-rich telomeric overhang might act like a semaphore to signal senescent cell cycle arrest. Short telomere length, telomeric single-strand breaks, low levels of loop-stabilizing proteins, or other factors may trigger this opening of the loop. Thus, both telomere shortening and the ultimate signalling into senescence are able to integrate different environmental and genetic factors, especially oxidative stress-mediated damage, which might otherwise become a thread to genomic stability. © 2001 Elsevier Science Ireland Ltd.

Publication metadata

Author(s): von Zglinicki T

Publication type: Review

Publication status: Published

Journal: Cancer Letters

Year: 2001

Volume: 168

Issue: 2

Pages: 111-116

ISSN (print): 0304-3835

ISSN (electronic): 1872-7980

URL: http://dx.doi.org/10.1016/S0304-3835(01)00546-8

DOI: 10.1016/S0304-3835(01)00546-8

PubMed id: 11403914

Share