title: Senescence and cell cycle control.
abstract: In response to various stresses, such as telomere shortening during continuous proliferation, oxidative stress, DNA damage and aberrant oncogene activation, normal cells undergo cellular senescence, which is a stable postmitotic state with particular morphology and metabolism. Signaling that induces senescence involves two major tumor suppressor cascades, i.e., the INK4a-Rb pathway and the ARF-p53 pathway. Diverse stimuli upregulate these interacting pathways, which orchestrate exit from the cell cycle. Recent studies have provided insights into substantial differences in senescence-inducing signals in primary cells of human and rodent origins. This review is focused on recent advances in understanding the roles of the tumor-suppressive pathways in senescence.
authors.affiliation: Department of Molecular Pharmacology and Biological Chemistry, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. kiyokawa@northwestern.edu
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Kiyokawa
mesh_terms: D000818:Animals; D002453:Cell Cycle; D016922:Cellular Senescence; D006801:Humans; D008954:Models, Biological