Replicative senescence revisited.

Richard Marcotte; Eugenia Wang

doi:10.1093/gerona/57.7.b257

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PubMed · 12084796

Replicative senescence revisited.

Richard Marcotte·Eugenia Wang

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Abstract

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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Animals Cell Cycle Cellular Senescence Cyclin-Dependent Kinase Inhibitor p16 Cyclin-Dependent Kinase Inhibitor p21 Cyclins Humans Retinoblastoma Protein Telomere Tumor Suppressor Protein p14ARF Tumor Suppressor Protein p53 Non-programmatic Journal Article Research Support, U.S. Gov't, P.H.S.Review

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Richard Marcotte, Eugenia Wang. 2002. Replicative senescence revisited.. https://doi.org/10.1093/gerona%2F57.7.b257

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