Molecular biology of HTLV-I: recent progress.
Molecular biology of HTLV-I: recent progress.
复制标题
HTLV-I 的分子生物学：最新进展。
DOI：
10.1097/00042560-199600001-00012
复制
发表时间：
1996
期刊：
影响因子：
--
通讯作者：
M. Yoshida
中科院分区：
文献类型：
--
作者：
M. Yoshida
人类T细胞淋巴营养病毒I型(HTLV-I)(1，2)是成人T细胞白血病(ATL)(3)和HTLV-I相关性脊髓病/热带痉挛麻痹(HAM/TSP)(4，5)的病原体。在ATL细胞中，前病毒整合的位置在患者中并不常见，尽管它们在个体内是克隆的(3)，因此病毒交易因子被认为是一种白血病因子。由于Tax可以使人T细胞永生化(7)，转化啮齿动物成纤维细胞系(8)，并在其转基因小鼠中诱导肿瘤(9)，Tax蛋白已被建议作为该交易因子的候选者(6)。TAX还被认为是病毒基因组转录的交易激活剂(10-12)，因此对病毒复制是必不可少的。Tax还激活许多特定的细胞基因，包括淋巴因子(13-15)、其一些受体(13)和核原癌基因(16，17)，因此这些基因中的一些被认为有助于T细胞永生化或转化。我们以前报道过Tax激活三个增强子(图1)，包括HTLV(18，19)的21个碱基对(BP)序列，白细胞介素2受体α基因的核因子(NF)-KB结合部位(20)，以及原癌基因c-fos和c-egr的血清反应元件(SRE)(21)。激活的机制被证明是TAX与结合到特定增强子的转录因子的结合。这些因子是cAMP反应元件结合(CREB)(22，23)或调节蛋白(CREM)蛋白(22)，与21-bp序列结合；NF-KB家族蛋白，包括与NF-KB结合部位的p50(24)、p52(25)、p65(26)和c-rel(26)；以及SRE(21)的血清反应因子。
Human T-cell lymphotrophic virus type I (HTLV-I)(1, 2) is a causative agent of adult T-cell leukemia (ATL)(3) and HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP)(4, 5). In ATL cells, the sites of provirus integration were not common among patients, although they were clonal within individuals (3), so the viral transacting factor was implicated as a leukemogenic factor. Tax protein has been proposed as a candidate for this transacting factor (6), since Tax can immortalize human T cells (7), transform rodent fibroblastic cell lines (8), and induce tumors in its transgenic mice (9). Tax is also identified as a transacting activator of viral genome transcription (10-12) and thus is essential for viral replication. Tax also activates many specific cellular genes, including lymphokines (13-15), some of their receptors (13), and nuclear protooncogenes (16, 17), so some of these genes have been thought to contribute to T-cell immortalization or transformation.We reported previously that Tax activates three enhancers (Fig. 1), including the 21-base-pair (bp) sequence of HTLV (18, 19), the nuclear factor (NF)-KB-binding site of the interleukin (IL)-2 receptor α gene (20), and the serum-responsive element (SRE) of the c-fos and c-egr protooncogenes (21). The mechanism of the activation was shown to be the binding of Tax to transcription factors that bind to specific enhancers. These factors are the cAMP-responsive element binding (CREB)(22, 23) or modulator (CREM) protein (22) that binds to the 21-bp sequence; NF-KB family proteins including p50 (24), p52 (25), p65 (26), and c-Rel (26) for the NF-KB-binding site; and the serum-responsive factor for the SRE (21).
DOI：
10.1073/pnas.89.15.7070
发表时间：
1992-08
影响因子：
11.1
作者：
Ling-Jun Zhao;C. Giam
通讯作者：
Ling-Jun Zhao;C. Giam
人 T 细胞白血病病毒 3 末端区域的表达。
DOI：
10.1126/science.6091270
发表时间：
1984
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Wachsman,W;Shimotohno,K;Clark,SC;Golde,DW;Chen,IS
通讯作者：
Chen,IS
DOI：
10.1073/pnas.86.9.3351
发表时间：
1989-05-01
影响因子：
11.1
作者：
GRASSMANN, R;DENGLER, C;HASELTINE, WA
通讯作者：
HASELTINE, WA