Tumor suppression by Ink4a-Arf:: progress and puzzles

被引：574
作者：
Lowe, SW
Sherr, CJ
机构：
[1] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA
[2] St Jude Childrens Res Hosp, Howard Hughes Med Inst, Dept Genet & Tumor Cell Biol, Memphis, TN 38105 USA
来源：
CURRENT OPINION IN GENETICS & DEVELOPMENT | 2003年 / 13卷 / 01期
关键词：
D O I：
10.1016/S0959-437X(02)00013-8
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
The two products of the Ink4a-Arf locus, p16(Ink4a) and p19(Arf) (p14(ARF) in humans), are potent tumor suppressors that regulate the activities of the retinoblastoma protein and the p53 transcription factor. These proteins form part of a signaling network that is disrupted in most, if not all, cancer cells. The Ink4a-Arf locus responds to stress signals, limiting cell proliferation and modulating oncogene-induced apoptosis. Recent evidence emerging from mouse tumor models distinguishes the activities of p16(Ink4a) and p19(Arf) in regulating tumor onset and identifies differences in their responsiveness to drugs.
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页码：77 / 83
页数：7
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