HIV-1信使核糖核酸3'末端加工受到真核起始因子3f、细胞周期蛋白依赖性激酶11和剪接因子9G8的独特调控。
HIV-1 mRNA 3' end processing is distinctively regulated by eIF3f, CDK11, and splice factor 9G8.
作者信息
Valente Susana T, Gilmartin Greg M, Venkatarama Krishnan, Arriagada Gloria, Goff Stephen P
机构信息
Howard Hughes Medical Institute, College of Physicians and Surgeons, Columbia University, HHSC 1310c, 701 West 168th Street, New York, NY 10032, USA.
出版信息
Mol Cell. 2009 Oct 23;36(2):279-89. doi: 10.1016/j.molcel.2009.10.004.
Abstract
A genetic screen previously identified the N-terminal 91 amino acids of the eukaryotic initiation factor 3 subunit f (N91-eIF3f) as a potent inhibitor of HIV-1 replication. Overexpression of N91-eIF3f or full-length eIF3f reduced the level of HIV-1 mRNAs in the infected cell. Here we show that N91-eIF3f and eIF3f act by specifically blocking the 3' end processing of the HIV-1 pre-mRNA both in vivo and in vitro. Furthermore, the results suggest that eIF3f mediates this restriction of HIV-1 expression through the previously unsuspected involvement of a set of factors that includes eIF3f, the SR protein 9G8, and the cyclin-dependent kinase 11 (CDK11). eIF3f affects HIV-1 3' end processing by modulating the sequence-specific recognition of the HIV-1 pre-mRNA by 9G8.
摘要
先前的一项基因筛选确定，真核起始因子3亚基f的N端91个氨基酸（N91-eIF3f）是HIV-1复制的有效抑制剂。N91-eIF3f或全长eIF3f的过表达降低了感染细胞中HIV-1 mRNA的水平。在此我们表明，N91-eIF3f和eIF3f通过在体内和体外特异性阻断HIV-1前体mRNA的3'端加工来发挥作用。此外，结果表明，eIF3f通过一组包括eIF3f、SR蛋白9G8和细胞周期蛋白依赖性激酶11（CDK11）的因子的先前未被怀疑的参与来介导对HIV-1表达的这种限制。eIF3f通过调节9G8对HIV-1前体mRNA的序列特异性识别来影响HIV-1 3'端加工。
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