Furnes C, Andresen V, Szilvay A M
Department of Molecular Biology, University of Bergen, Bergen, Norway.
Arch Virol. 2008;153(2):357-62. doi: 10.1007/s00705-007-1095-x. Epub 2007 Dec 20.
The HIV-1 wild-type Rev and the negative oligomerization-defective mutant RevM4 were fused to enhanced green fluorescent protein (EGFP) and the tetrameric red fluorescent protein (DsRed1) followed by examination of their intracellular localization and Rev activity. As previously shown, fusion of EGFP to Rev and RevM4 did not affect the biological activity. Fusion of DsRed1 to Rev inhibited activity, and interestingly, fusion of DsRed1 to RevM4 restored activity. Based on these results, a model is proposed suggesting how RevM4-DsRed1 is able to rescue Rev activity through oligomerization on the viral RNA.
将HIV-1野生型Rev和负性寡聚化缺陷突变体RevM4与增强型绿色荧光蛋白（EGFP）和四聚体红色荧光蛋白（DsRed1）融合，随后检测它们在细胞内的定位和Rev活性。如先前所示，EGFP与Rev和RevM4的融合不影响生物活性。DsRed1与Rev的融合抑制活性，有趣的是，DsRed1与RevM4的融合恢复了活性。基于这些结果，提出了一个模型，表明RevM4-DsRed1如何通过在病毒RNA上的寡聚化来挽救Rev活性。
