COOPERATION BETWEEN BOVINE LEUKEMIA-VIRUS TRANSACTIVATOR PROTEIN AND HA-RAS ONCOGENE PRODUCT IN CELLULAR-TRANSFORMATION
COOPERATION BETWEEN BOVINE LEUKEMIA-VIRUS TRANSACTIVATOR PROTEIN AND HA-RAS ONCOGENE PRODUCT IN CELLULAR-TRANSFORMATION
复制标题
DOI：
10.1002/j.1460-2075.1990.tb08277.x
复制
发表时间：
1990-05-01
期刊：
影响因子：
11.4
通讯作者：
KETTMANN, R
中科院分区：
文献类型：
--
作者：
WILLEMS, L;HEREMANS, H;KETTMANN, R
人嗜T淋巴细胞病毒（HTLV-I和-II）和牛白血病病毒（BLV）表达能够增加长末端重复序列（LTR）指导的病毒表达的反式激活蛋白。这些反式作用因子被认为与这些病毒诱导白血病有关。体外转染BLV反式激活因子p34 tax和Ha-ras使大鼠胚胎成纤维细胞永生化和转化。转化的细胞在裸鼠中诱发肿瘤。这些数据强调了p34 tax在体内肿瘤发生中的因果作用。
Human T-lymphotropic viruses (HTLV-I and -II) and bovine leukemia virus (BLV) express transactivator proteins able to increase long terminal repeat (LTR) directed viral expression. These transacting factors are thought to be involved in the induction of leukaemia by these viruses. Transfection of BLV transactivator p34tax together with Ha-ras immortalizes and transforms rat embryo fibroblasts, in vitro. The transformed cells induce tumours in nude mice. These data emphasize the causal role exerted by p34tax in in vivo tumorigenesis.