Mechanisms of HTLV-1 transformation

被引:16
作者
Kehn, K
Berro, R
de la Fuente, C
Strouss, K
Ghedin, E
Dadgar, S
Bottazzi, ME
Pumfery, A
Kashanchi, F
机构
[1] George Washington Univ, Sch Med & Hlth Sci, Dept Biochem & Mol Biol, Washington, DC 20037 USA
[2] George Washington Univ, Sch Med & Hlth Sci, Dept Microbiol & Trop Med, Washington, DC 20037 USA
[3] Inst Genom Res TIGR, Rockville, MD 20850 USA
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2004年 / 9卷
关键词
HTLV-1; oncogenesis; tax; ATL; cell cycle; transcription; accessory proteins; apoptosis; review;
D O I
10.2741/1401
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-1 is the etiological agent of the fatal disease adult T-cell leukemia. The virus encodes many proteins including several accessory proteins, p12(I), p13(II), p27(I), and p30(II), whose roles have recently begun to be elucidated. These accessory proteins are important in T-cell activation, transcriptional regulation, viral persistence, and virus assembly. The viral oncogene Tax is thought to be largely responsible for tumorigenesis, although the precise mechanisms underlying transformation are not completely understood. Tax has a profound impact on transcription, cell growth regulation, genomic stability and apoptosis. This review will provide possible contributions of the accessory proteins to transformation as well as highlight the alterations of the above-mentioned cellular events by Tax. Animal models of both Tax and the accessory proteins are also included based on the essential information on the transformation process in vivo that they provide.
引用
收藏
页码:2347 / 2372
页数:26
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