Roy S, Katze M G, Parkin N T, Edery I, Hovanessian A G, Sonenberg N
Department of Biochemistry, McGill University, Montreal, Canada.
Science. 1990 Mar 9;247(4947):1216-9. doi: 10.1126/science.2180064.
The tat-responsive region (TAR) of the human immunodeficiency virus-1 (HIV-1) exhibits a trans-inhibitory effect on translation in vitro by activating the interferon-induced 68-kilodalton protein kinase (p68 kinase). Productive infection by HIV-1 was shown to result in a significant decrease in the amount of cellular p68 kinase. The steady-state amount of p68 kinase was also reduced in interferon-treated HeLa cell lines stably expressing tat, as compared to the amount of the kinase in interferon-treated control HeLa cells. Thus, the potential translational inhibitory effects of the TAR RNA region mediated by activation of p68 kinase may be downregulated by tat during productive HIV-1 infection.
人类免疫缺陷病毒1型（HIV-1）的反式激活应答区域（TAR）通过激活干扰素诱导的68千道尔顿蛋白激酶（p68激酶）在体外对翻译表现出反式抑制作用。已表明HIV-1的有效感染会导致细胞p68激酶量显著减少。与经干扰素处理的对照HeLa细胞中的激酶量相比，在稳定表达tat的经干扰素处理的HeLa细胞系中，p68激酶的稳态量也减少。因此，在HIV-1有效感染期间，tat可能会下调由p68激酶激活介导的TAR RNA区域的潜在翻译抑制作用。
