QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online February 21, 2007
doi: 10.1242/10.1242/jcs.03397

This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Multani, A. S. Articles by Chang, S. Search for Related Content PubMed PubMed Citation Articles by Multani, A. S. Articles by Chang, S.

WRN at telomeres: implications for aging and cancer

Department of Molecular Genetics, U.T. M.D. Anderson Cancer Center, Houston, TX 77030, USA

^* Author for correspondence (e-mail: schang{at}manderson.org)

Accepted 5 December 2006

Werner Syndrome (WS) is a premature aging syndrome characterized by early onset of age-related pathologies and cancer. Since WS is due to a single gene defect, it has attracted much interest from researchers seeking to understand pathways that contribute to cancer and aging at cellular and molecular levels. The protein mutated in WS, WRN, appears to play a major role in genome stability, particularly during DNA replication and telomere metabolism. Much of the pathophysiology associated with WS, including the rapid onset of cellular senescence, early cancer onset and premature aging, can be attributed to a defect in telomere maintenance. Recent genetic evidence from the mTerc^–/– Wrn^–/– mouse demonstrates that mice with critically shortened telomeres display aging phenotypes reminiscent of human WS, further reinforcing the notion that telomere dysfunction is required for the manifestation of aging pathophysiologies in the setting of WRN deficiency.

Key words: Werner Syndrome, Telomere, DNA damage, Aging, Cancer

This article has been cited by other articles:

				G. Aubert and P. M. Lansdorp Telomeres and Aging Physiol Rev, April 1, 2008; 88(2): 557 - 579. [Abstract] [Full Text] [PDF]

				L. M. Pirzio, P. Pichierri, M. Bignami, and A. Franchitto Werner syndrome helicase activity is essential in maintaining fragile site stability J. Cell Biol., January 28, 2008; 180(2): 305 - 314. [Abstract] [Full Text] [PDF]

				R. M. Brosh Jr and V. A. Bohr Human premature aging, DNA repair and RecQ helicases Nucleic Acids Res., December 3, 2007; 35(22): 7527 - 7544. [Abstract] [Full Text] [PDF]