Hope T J, Bond B L, McDonald D, Klein N P, Parslow T G
Department of Pathology, University of California, San Francisco 94143-0506.
J Virol. 1991 Nov;65(11):6001-7. doi: 10.1128/JVI.65.11.6001-6007.1991.
The human immunodeficiency virus type 1 Rev and human T-cell leukemia virus type I Rex transactivators are posttranscriptional regulatory proteins that promote retroviral gene expression by interacting with specific viral mRNAs. Rev and Rex have markedly dissimilar amino acid sequences and RNA target specificities but are thought to act through the same cellular pathway. In this report, we demonstrate that short peptide domains which are required for effector activity in Rev and Rex are functionally interchangeable. Activity of these effector domains depends upon a previously unrecognized tetrapeptide motif that is present in both Rev and Rex and also in analogous proteins from other complex retroviruses. The conserved effector motif may mediate essential interactions of Rev, Rex, and other transactivators of this type with a common cellular cofactor.
1型人类免疫缺陷病毒Rev和1型人类T细胞白血病病毒Rex反式激活因子是转录后调节蛋白,它们通过与特定病毒mRNA相互作用来促进逆转录病毒基因表达。Rev和Rex具有明显不同的氨基酸序列和RNA靶标特异性,但被认为通过相同的细胞途径发挥作用。在本报告中,我们证明了Rev和Rex中效应子活性所需的短肽结构域在功能上是可互换的。这些效应子结构域的活性取决于一个先前未被识别的四肽基序,该基序存在于Rev和Rex中,也存在于其他复杂逆转录病毒的类似蛋白中。保守的效应子基序可能介导Rev、Rex和此类其他反式激活因子与共同细胞辅因子的关键相互作用。