Kubota S, Nosaka T, Furuta R, Maki M, Hatanaka M
Institute for Virus Research, Kyoto University, Japan.
Biochem Biophys Res Commun. 1991 Aug 15;178(3):1226-32. doi: 10.1016/0006-291x(91)91024-7.
A nucleolar localizing rev gene mutant M10 of human immunodeficiency virus type 1 (HIV-1) lost a Rev function completely, instead, gained a Rex activity of human T cell leukemia virus type 1 (HTLV-1). The obtained compatibility between Rev M10 and Rex with their own nucleolar targeting signal (NOS) suggests a common molecular mechanism of their post-transcriptional regulation, despite no sequence similarities of both proteins and their responsive RNA elements, respectively.
人类免疫缺陷病毒1型(HIV-1)的一种核仁定位的Rev基因突变体M10完全丧失了Rev功能,相反,却获得了人类T细胞白血病病毒1型(HTLV-1)的Rex活性。尽管Rev M10和Rex这两种蛋白质及其相应的RNA元件在序列上没有相似性,但它们与自身核仁靶向信号(NOS)之间获得的兼容性表明了它们转录后调控的共同分子机制。