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The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 57:B257-B269 (2002)
© 2002 The Gerontological Society of America

Replicative Senescence Revisited

Richard Marcottea and Eugenia Wangb

a Bloomfield Center for Research in Aging, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital, and Department of Medicine, McGill University, Montréal, Québec, Canada.
b Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Kentucky

Eugenia Wang, Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Louisville, KY 40292 E-mail: eugenia.wang{at}louisville.edu.

Decision Editor: James R. Smith, PhD

Forty years after its discovery, replicative senescence remains a rich source of information about cell-cycle regulation and the progression from a normal to a transformed phenotype. Effectors of this growth-arrested state are being discovered at a great pace. This review discusses the latest findings on the players responsible for establishing replicative senescence, as well as the associated telomere shortening.




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