Senescence and cell cycle control

Hiroaki Kiyokawa*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapter

9 Scopus citations

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.

Original languageEnglish (US)
Title of host publicationCell Cycle Regulation
EditorsPhilipp Kaldiss
Pages257-270
Number of pages14
DOIs
StatePublished - Dec 11 2006

Publication series

NameResults and Problems in Cell Differentiation
Volume42
ISSN (Print)0080-1844
ISSN (Electronic)1861-0412

ASJC Scopus subject areas

  • Developmental Biology
  • Cell Biology

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