期刊
CELL CYCLE
卷 11, 期 22, 页码 4147-4151出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.22589
关键词
p53; p16(INK4A); HRAS(G12V); NRAS(Q61R); BRAF(V600E); DNA damage; DNA damage response; C-MYC; thymidylate synthase; ribonucleotide reductase; deoxyribonucleotides
类别
资金
- NCI NIH HHS [R01 CA120244] Funding Source: Medline
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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