Robek M D, Ratner L
Departments of Medicine, Pathology, and Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
J Virol. 2000 Dec;74(24):11988-92. doi: 10.1128/jvi.74.24.11988-11992.2000.
The human T-cell leukemia virus type 1 (HTLV-1) Tax oncoprotein is a 40-kDa nuclear phosphoprotein which functions in the viral replication cycle as a transcriptional trans-activator of the viral long terminal repeat. Tax interacts with a variety of different transcription factors, including the CREB binding protein (CBP)/p300 family of transcriptional accessory proteins. We demonstrate that a Tax mutant defective for the CBP/p300 interaction retains the capacity to immortalize primary human T lymphocytes when it is expressed from a functional molecular clone of HTLV-1. Thus, immortalization of HTLV-1-infected cells appears to be independent of Tax-induced alterations in CBP/p300 function.
人类1型T细胞白血病病毒(HTLV-1)的Tax癌蛋白是一种40 kDa的核磷蛋白,在病毒复制周期中作为病毒长末端重复序列的转录反式激活因子发挥作用。Tax与多种不同的转录因子相互作用,包括CREB结合蛋白(CBP)/p300转录辅助蛋白家族。我们证明,一个在与CBP/p300相互作用方面存在缺陷的Tax突变体,当它从HTLV-1的功能性分子克隆中表达时,仍保留使原代人T淋巴细胞永生化的能力。因此,HTLV-1感染细胞的永生化似乎独立于Tax诱导的CBP/p300功能改变。