期刊
EUROPEAN JOURNAL OF BIOCHEMISTRY
卷 268, 期 10, 页码 2784-2791出版社
WILEY
DOI: 10.1046/j.1432-1327.2001.02228.x
关键词
cellular senescence; cyclin-dependent kinase inhibitors; DNA repair proteins; E2F1; p14/ARF; p21; p53; PML; RAS; telomeres; tumor suppressors
Many normal cells respond to potentially oncogenic stimuli by undergoing cellular senescence, a state of irreversibly arrested proliferation and altered differentiated function. Cellular senescence very likely evolved to suppress tumorigenesis. In support of this idea, it is regulated by several tumor suppressor genes. At the heart of this regulation is p53. p53 is essential for the senescence response to short telomeres, DNA damage, oncogenes and supraphysiological mitogenic signals, and overexpression of certain tumor suppressor genes. Despite the well-documented central role for p53 in the senescence response, many questions remain regarding how p53 senses senescence-inducing stimuli and how it elicits the senescent phenotype.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据