Vif是HIV-1逆转录酶的辅助因子，可促进无碱基位点的绕过。
Vif is an auxiliary factor of the HIV-1 reverse transcriptase and facilitates abasic site bypass.
作者信息
Cancio Reynel, Spadari Silvio, Maga Giovanni
机构信息
Istituto di Genetica Molecolare IGM - CNR, via Abbiategrasso 207, I-27100 Pavia, Italy.
出版信息
Biochem J. 2004 Nov 1;383(Pt. 3):475-82. doi: 10.1042/BJ20040914.
Abstract
The HIV-1 accessory protein Vif was found to modulate the RNA- and DNA-dependent DNA synthesis activity of the viral RT (reverse transcriptase) in two ways: (i) it stimulated the binding of the viral RT to the primer by increasing the association rate kcat/K(m) and by decreasing the thermodynamic barrier DeltaH([ES]) for complex formation, and (ii) it increased the polymerization rate of HIV-1 RT. A Vif mutant lacking the final 56 amino acids at the C-terminus failed to stimulate the viral RT. On the other hand, another Vif mutant lacking the first 43 amino acids at the N-terminus, which are involved in RNA binding and interaction with the viral protease, was able to stimulate RT activity. In addition, Vif was found to promote the bypass of an abasic site by HIV-1 RT.
摘要
人们发现，HIV-1辅助蛋白Vif通过两种方式调节病毒逆转录酶（RT）的RNA依赖性和DNA依赖性DNA合成活性：（i）它通过提高结合速率kcat/K(m)和降低复合物形成的热力学屏障ΔH([ES])来刺激病毒RT与引物的结合，以及（ii）它提高HIV-1 RT的聚合速率。一个在C末端缺少最后56个氨基酸的Vif突变体无法刺激病毒RT。另一方面，另一个在N末端缺少最初43个氨基酸（参与RNA结合和与病毒蛋白酶相互作用）的Vif突变体能够刺激RT活性。此外，人们发现Vif能促进HIV-1 RT绕过无碱基位点。
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