Journal
CELL CYCLE
Volume 4, Issue 10, Pages 1364-1368Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.4.10.2104
Keywords
telomere; p16INK4a; p53; TRF2; senescence
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Funding
- NIA NIH HHS [AG16642] Funding Source: Medline
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Telomere damage resulting from telomere shortening can potentially suppress tumorigenesis by permanently arresting or eliminating incipient cancer cells. Dysfunctional telomeres activate the canonical DNA damage response pathway, resulting in a p53-mediated G(1)/S arrest and senescence or apoptosis. Experimental induction of telomere damage through inhibition of the telomeric protein TRF2 recapitulates aspects of telomere attrition, including a p53-mediated cell cycle arrest. Using this system, we have shown that telomere damage can also elicit a G(1)/S arrest through the RB-regulator p16INK4a, especially in cells lacking p53 function. Here we discuss the significance of p16INK4a as a second effector of the telomere damage response.
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