Human T-cell leukemia virus type 2 (HTLV-2) Tax protein transforms a rat fibroblast cell line but less efficiently than HTLV-1 Tax

被引:63
作者
Endo, K
Hirata, A
Iwai, K
Sakurai, M
Fukushi, M
Oie, M
Higuchi, M
Hall, WW
Gejyo, F
Fujii, M
机构
[1] Niigata Univ, Grad Sch Med & Dent Sci, Div Virol, Niigata 9518510, Japan
[2] Niigata Univ, Grad Sch Med & Dent Sci, Div Clin Nephrol & Rheumatol, Niigata 9518510, Japan
[3] Univ Coll Dublin, Conway Inst Biomol & Biomed Res, Dept Med Microbiol, Belfield, Ireland
关键词
D O I
10.1128/JVI.76.6.2648-2653.2002
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Human T-cell leukemia virus type I (HTLV-1) and HTLV-2 are retroviruses with similar biological properties. Whereas HTLV-1 is the causative agent of an aggressive T-cell leukemia, HTLV-2 has been associated with only a few cases of lymphoproliferative disorders. Taxi and Tax2 are the transcriptional activators of HTLV-1 and HTLV-2, respectively. Here we show that Tax2 transformed a Rat-1 fibroblast cell line to form colonies in soft agar, but the size and number of the colonies were lower than those of Taxi. Use of a chimeric Tax protein showed that the C-terminal amino acids 300 to 353 were responsible for the high transforming activity of Taxi. Activation of cellular genes by Taxi through transcription factor NF-kappaB is reportedly essential for the transformation of Rat-1 cells. Tax2 also activated the transcription through NF-kappaB in Rat-1 cells, and such activity was equivalent to that induced by Taxi. Thus, the high transforming activity of Taxi is mediated by mechanisms other than NF-kappaB activation. Our results showed that Tax2 has a lower transforming activity than Taxi and suggest that the high transforming activity of Taxi is involved in the leukemogenic property of HTLV-1.
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页码:2648 / 2653
页数:6
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