Journal
CELL CYCLE
Volume 11, Issue 22, Pages 4147-4151Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.22589
Keywords
p53; p16(INK4A); HRAS(G12V); NRAS(Q61R); BRAF(V600E); DNA damage; DNA damage response; C-MYC; thymidylate synthase; ribonucleotide reductase; deoxyribonucleotides
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Funding
- NCI NIH HHS [R01 CA120244] Funding Source: Medline
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Oncogene-induced senescence (OIS) is a fail-safe mechanism that is developed to suppress cell proliferation caused by aberrant activation of oncoproteins in normal cells. Most of the available literature considers senescence to be caused by activated RAS or RAF proteins. In the current review, we will discuss some of the controversial aspects of RAS- or RAF-induced senescence in different types of normal cells: are tumor suppressors important for OIS? What is the role of DNA damage in OIS? Are there different types of OIS?
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