Chang P Y, Stellrecht K, Melana S, Pogo B G
Department of Microbiology, Mount Sinai School of Medicine, New York, NY 10029.
Virus Res. 1994 Nov;34(2):127-38. doi: 10.1016/0168-1702(94)90095-7.
Previous reports showed transactivation of the long terminal repeat (LTR) of HIV-1 in Jurkat cells persistently infected with vaccinia virus. In this communication, electrophoretic mobility shift assays were used to characterize the elements in HIV-1 LTR which might be responsible for the mechanism of transactivation. The results indicated that two elements, those for binding NF-kB and NFAT-1, were able to interact with nuclear extracts derived from Jurkat cells persistently infected with vaccinia virus, suggesting that they may play a role in the transactivation of HIV-1 LTR.
先前的报告显示，在持续感染痘苗病毒的Jurkat细胞中，HIV-1的长末端重复序列（LTR）会被反式激活。在本通讯中，采用电泳迁移率变动分析来鉴定HIV-1 LTR中可能与反式激活机制有关的元件。结果表明，两个元件，即与NF-kB和NFAT-1结合的元件，能够与来自持续感染痘苗病毒的Jurkat细胞的核提取物相互作用，这表明它们可能在HIV-1 LTR的反式激活中发挥作用。
