Replicative senescence revisited.
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.
Marcotte
Richard
R
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.
Wang
Eugenia
E
D000818:Animals; D002453:Cell Cycle; D016922:Cellular Senescence / Q000502:physiology*; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000502:physiology; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000502:physiology; D006801:Humans; D016160:Retinoblastoma Protein / Q000502:physiology; D016615:Telomere; D025803:Tumor Suppressor Protein p14ARF / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000502:physiology
C493956:CDKN1A protein, human; C417743:Cdkn2a protein, mouse; D019941:Cyclin-Dependent Kinase Inhibitor p16; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D016160:Retinoblastoma Protein; D025803:Tumor Suppressor Protein p14ARF; D016159:Tumor Suppressor Protein p53