Human T-cell leukemia virus type II Rex binding and activity require an intact splice donor site and a specific RNA secondary structure.
Human T-cell leukemia virus type II Rex binding and activity require an intact splice donor site and a specific RNA secondary structure.
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人类 T 细胞白血病病毒 II 型 Rex 的结合和活性需要完整的剪接供体位点和特定的 RNA 二级结构。
DOI：
10.1128/jvi.65.12.6645-6653.1991
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发表时间：
1991
影响因子：
5.4
通讯作者：
Rosenblatt,JD
中科院分区：
文献类型：
--
作者：
Black,AC;Ruland,CT;Yip,MT;Luo,J;Tran,B;Kalsi,A;Quan,E;Aboud,M;Chen,IS;Rosenblatt,JD
人类T细胞白血病病毒II型（HTLV-II）调节蛋白雷克斯通过长末端重复序列中的雷克斯应答元件（RxRE）作用，增加未剪接gag-pol mRNA的细胞质水平。纯化的雷克斯蛋白结合长末端重复mRNA。在这里，使用免疫结合试验来测量结合的雷克斯蛋白质突变RxRE RNA，我们表明，有效的雷克斯结合需要一个茎-凸起-环RNA二级结构（核苷酸[nt] 465至500）和特定的序列都在茎-凸起（nt 470至476）和保守的上游剪接供体位点（nt 449至455）。瞬时转染表达系统中的雷克斯功能与雷克斯蛋白-RxRE RNA结合相关。HTLV-II雷克斯与HTLV-II剪接供体位点直接相互作用的能力表明，HTLV-II雷克斯可能部分通过抑制剪接来增加未剪接的gag-pol mRNA的表达。
The human T-cell leukemia virus type II (HTLV-II) regulatory protein Rex augments cytoplasmic levels of unspliced gag-pol mRNA by acting through a Rex-responsive element (RxRE) in the long terminal repeat. Purified Rex protein binds to long terminal repeat mRNA. Here, using an immunobinding assay to measure the binding of Rex protein to mutated RxRE RNAs, we show that efficient Rex binding requires a stem-bulge-loop RNA secondary structure (nucleotides [nt] 465 to 500) and specific sequences both within the stem-bulge (nt 470 to 476) and within a conserved upstream splice donor site (nt 449 to 455). Rex function in a transient transfection expression system correlates with Rex protein-RxRE RNA binding. The ability of HTLV-II Rex to interact directly with the HTLV-II splice donor site suggests that HTLV-II Rex may increase expression of unspliced gag-pol mRNA, in part, by inhibiting splicing.