Journal
GENES & DEVELOPMENT
Volume 28, Issue 2, Pages 99-114Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.235184.113
Keywords
senescence; aging; DNA damage; oncogenes; tumor suppressors; inflammation; metabolism
Categories
Funding
- University of Cambridge, Cancer Research UK, Hutchison Whampoa
- Human Frontier Science Program
- Cancer Research UK Clinician Scientist Fellowship
- Cancer Research UK [15890] Funding Source: researchfish
Ask authors/readers for more resources
Cellular senescence is a stress response that accompanies stable exit from the cell cycle. Classically, senescence, particularly in human cells, involves the p53 and p16/Rb pathways, and often both of these tumor suppressor pathways need to be abrogated to bypass senescence. In parallel, a number of effector mechanisms of senescence have been identified and characterized. These studies suggest that senescence is a collective phenotype of these multiple effectors, and their intensity and combination can be different depending on triggers and cell types, conferring a complex and diverse nature to senescence. Series of studies on senescence-associated secretory phenotype (SASP) in particular have revealed various layers of functionality of senescent cells in vivo. Here we discuss some key features of senescence effectors and attempt to functionally link them when it is possible.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available