Sci. Aging Knowl. Environ., 28 June 2006
Vol. 2006, Issue 10, p. pe18
[DOI: 10.1126/sageke.2006.10.pe18]

PERSPECTIVES

WRN's Tenth Anniversary

Fuki M. Hisama, Vilhelm A. Bohr, and Junko Oshima

The authors are in the Department of Neurology at Yale University, New Haven, CT 06520, USA (F.M.H.), the Laboratory of Molecular Gerontology at the National Institutes on Aging, the National Institutes of Health, Baltimore, MD 21224, USA (V.A.B.), and the Department of Pathology at the University of Washington, Seattle, WA 98195, USA (J.O.). E-mail: fuki.hisama{at}yale.edu (F.M.H.), vbohr{at}nih.gov (V.A.B.), picard{at}u.washington.edu (J.O.)

http://sageke.sciencemag.org/cgi/content/full/2006/10/pe18

Key Words: Werner syndrome • progeroid • WRN • RecQ helicase • exonuclease • telomere • genome instability • DNA repair

Abstract: Werner syndrome (WS) is a segmental progeroid syndrome in which patients display pleiotropic features of aging seen in the normal population. The advent of positional cloning in the 1990s markedly accelerated the identification of human disease-causing genes. In 1996, mutations in WRN, which was shown to encode a new, putative member of the family of RecQ DNA helicases, were identified in four patients as the cause of WS. Ten years after the identification of WRN, what have we learned about its role in WS, and its contribution to normal aging?

Citation: F. M. Hisama, V. A. Bohr, J. Oshima, WRN's Tenth Anniversary. Sci. Aging Knowl. Environ. 2006 (10), pe18 (2006).

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