Srinivasan Viswanathan, Komatsu Takashi, Ballestas Mary E, Kaye Kenneth M
Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
J Virol. 2004 Dec;78(24):14033-8. doi: 10.1128/JVI.78.24.14033-14038.2004.
In latent infection, Kaposi's sarcoma-associated herpesvirus (KSHV) latency-associated nuclear antigen 1 (LANA1)-specific binding to KSHV terminal repeat DNA mediates multicopy episome persistence. We now use electrophoretic mobility shift assays to investigate LANA1 binding to its 20-bp cognate sequence. Mutations at positions 6, 7, and 8 ((6)CCC(8)) severely reduced LANA1 binding, whereas mutations at other positions only modestly reduced binding. Since (6)CCC(8) is in the 5' half of an inverted repeat sequence, these results are consistent with an asymmetric role for the inverted repeat in LANA1 binding.
在潜伏感染中,卡波西肉瘤相关疱疹病毒(KSHV)的潜伏相关核抗原1(LANA1)与KSHV末端重复DNA的特异性结合介导了多拷贝附加体的持久性。我们现在使用电泳迁移率变动分析来研究LANA1与其20个碱基对的同源序列的结合。第6、7和8位((6)CCC(8))的突变严重降低了LANA1的结合,而其他位置的突变仅适度降低了结合。由于(6)CCC(8)位于反向重复序列的5'半部分,这些结果与反向重复在LANA1结合中的不对称作用一致。