Document Detail

Telomeres, senescence and cellular radiation response.
MedLine Citation:
PMID:  9284959     Owner:  NLM     Status:  MEDLINE    
Telomeres shield the ends of chromosomes from degradation and end-to-end fusions. They shorten at each cell division and when they reach a critically short length, cells arrest in the G1 phase of the cell cycle and undergo senescence. This effectively limits the proliferative potential of cells. Senescence functions as a tumour suppressor mechanism and appears to contribute to the process of ageing. If senescence is circumvented by tumour viruses, proliferation is re-initiated until cells enter crisis. Activation of telomerase prevents telomere attrition and cells become immortal. Cellular response to ionizing radiation involves induction of cell cycle checkpoint arrests and programmed cell death. Because radiation produces double strand breaks in DNA, which cause telomere-less chromosome ends, radiation response appears to be the result of inappropriate induction of cellular senescence mechanisms.
N E Crompton
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Cellular and molecular life sciences : CMLS     Volume:  53     ISSN:  1420-682X     ISO Abbreviation:  Cell. Mol. Life Sci.     Publication Date:  1997 Jul 
Date Detail:
Created Date:  1997-10-01     Completed Date:  1997-10-01     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9705402     Medline TA:  Cell Mol Life Sci     Country:  SWITZERLAND    
Other Details:
Languages:  eng     Pagination:  568-75     Citation Subset:  IM    
Institute of Medical Radiobiology, Villigen-PSI, Switzerland.
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MeSH Terms
Cell Aging*
Cell Cycle / radiation effects
Cell Transformation, Neoplastic
DNA Damage
DNA Replication
Enzyme Activation
Oncogenic Viruses / physiology
Radiation, Ionizing*
Signal Transduction
Telomerase / metabolism
Telomere / physiology*,  radiation effects*
Reg. No./Substance:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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