Work

p16INK4a as a Second Effector of the Telomere Damage Pathway

Year: 2005

Type: review

Abstract: 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.

Source: Cell Cycle

DOI: 10.4161/cc.4.10.2104

Authors: Jacqueline J.L. Jacobs, Titia de Lange

Institutions: The Netherlands Cancer Institute, Rockefeller University

Language: English

Topic: Telomeres, Telomerase, and Senescence

Subfield: Cell Biology

Field: Biochemistry, Genetics and Molecular Biology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: bronze

Funders: National Institutes of Health, National Institute on Aging