Akagi T, Ono H, Nyunoya H, Shimotohno K
Virology Division, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
Oncogene. 1997 May 1;14(17):2071-8. doi: 10.1038/sj.onc.1201045.
Tax1, a transcriptional trans-activator of the Human T-cell leukemia virus type I (HTLV-I), induces the expression of many cellular genes through interaction with at least three distinct cellular transcription factors; CREB/ATF, NF-kappaB, and SRF. This Tax1-induced activation of cellular genes is considered to be a critical event in T-cell transformation by HTLV-I. To elucidate the role of each Tax1-inducible transcriptional pathway in T-cell transformation, we introduced Tax1 mutants with different trans-activating phenotypes into peripheral blood lymphocytes (PBL) by retroviral vectors. Analysis of these PBLs revealed that activation of the NF-kappaB pathway is sufficient to promote the growth response to IL-2. However, for the clonal expansion of CD4+ T-cells, which is a characteristic result of HTLV-I infection, activation of the CREB/ATF and SRF pathways is also required.
Tax1是I型人类T细胞白血病病毒(HTLV-I)的转录反式激活因子,它通过与至少三种不同的细胞转录因子(CREB/ATF、NF-κB和SRF)相互作用来诱导许多细胞基因的表达。这种Tax1诱导的细胞基因激活被认为是HTLV-I导致T细胞转化的关键事件。为了阐明每个Tax1诱导的转录途径在T细胞转化中的作用,我们通过逆转录病毒载体将具有不同反式激活表型的Tax1突变体导入外周血淋巴细胞(PBL)。对这些PBL的分析表明,NF-κB途径的激活足以促进对IL-2的生长反应。然而,对于HTLV-I感染的特征性结果——CD4+ T细胞的克隆扩增,CREB/ATF和SRF途径的激活也是必需的。