Cell cycle dysregulation by HTLV-I: Role of the tax oncoprotein

被引:38
作者
Neuveut, C
Jeang, KT
机构
[1] NIAID, Mol Virol Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA
[2] Inst Pasteur, Lab Recombinaison & Express Genet, F-75724 Paris 15, France
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2002年 / 7卷
关键词
cell cycle regulation; cellular transformation; HTLV-I; adult T-cell leukemia; tax oncoprotein; MAD1; p53; review;
D O I
10.2741/neuveut
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
HTLV-I is a human retrovirus which is the etiological agent for adult T-cell leukemia. The virus encodes a 40 kDa oncoprotein, Tax, which has no cellular counterpart. Findings from several laboratories over the past decade have shown that over-expression of the Tax oncoprotein is wholly sufficient to transform animal cells. Emerging evidence supports that Tax transforms cells through dysregulation of several cell cycle checkpoints. Here, we review extant data on how Tax targets cyclins, inhibitors of cyclin dependant kinase, as well as cellular sentries for DNA-damage.
引用
收藏
页码:D157 / D163
页数:7
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