title: Cellular senescence, telomere recombination and maintenance.
abstract: Cellular senescence can be activated by various types of stressful stimuli, including telomere shortening, oncogenic or tumor suppressor signals, and DNA damage. Progressive telomere shortening in successive cell divisions induces senescence due to the loss of terminal sequences during DNA replication. Maintenance of the telomere sequences at human chromosome ends is essential for immortalized cells to escape from the normal limitations of the proliferation capacity. In this article, the molecular and functional details of telomere maintenance and cellular senescence are reviewed, including the signals that trigger senescence, telomere capping, and the telomere length maintenance mechanisms.
authors.affiliation: Department of Radiation Oncology, Washington University School of Medicine, St. Louis, MO 63108, USA. qyang@wustl.edu
authors.forename: Q
authors.initials: Q
authors.lastname: Yang
mesh_terms: D002455:Cell Division; D016922:Cellular Senescence / Q000235:genetics*; D004247:DNA / Q000235:genetics; D004249:DNA Damage; D004273:DNA, Neoplasm / Q000235:genetics; D005347:Fibroblasts / Q000166:cytology* / Q000502:physiology; D006801:Humans; D009369:Neoplasms / Q000473:pathology; D011995:Recombination, Genetic; D019098:Telomerase / Q000235:genetics; D016615:Telomere / Q000235:genetics*; D034501:Telomere-Binding Proteins / Q000235:genetics
chemical_list: D004273:DNA, Neoplasm; D034501:Telomere-Binding Proteins; D004247:DNA; D019098:Telomerase