Vif Proteins of Human and Simian Immunodeficiency Viruses Require Cellular CBFβ To Degrade APOBEC3 Restriction Factors

被引：62
|
作者：
Hultquist, Judd F. [1 ,2 ]
Binka, Mawuena [3 ]
LaRue, Rebecca S. [1 ]
Simon, Viviana [3 ,4 ,5 ]
Harris, Reuben S. [1 ,2 ]
机构：
[1] Univ Minnesota, Dept Biochem Mol Biol & Biophys, Inst Mol Virol, Ctr Genome Engn,Masonic Canc Ctr, Minneapolis, MN 55455 USA
[2] Univ Minnesota, Dept Mol Cellular Dev Biol & Genet, Minneapolis, MN USA
[3] Mt Sinai Sch Med, Dept Microbiol, New York, NY USA
[4] Mt Sinai Sch Med, Global Hlth & Emerging Pathogens Inst, New York, NY USA
[5] Mt Sinai Sch Med, Dept Med, Div Infect Dis, New York, NY USA
来源：
JOURNAL OF VIROLOGY | 2012年 / 86卷 / 05期
关键词：
HIV-1; UBIQUITINATION; COMPLEX;
D O I：
10.1128/JVI.06950-11
中图分类号：
Q93 [微生物学];
学科分类号：
071005 ; 100705 ;
摘要：
HIV-1 requires the cellular transcription factor CBF beta to stabilize its accessory protein Vif and promote APOBEC3G degradation. Here, we demonstrate that both isoforms of CBF beta allow for increased steady-state levels of Vif, enhanced APOBEC3G degradation, and increased viral infectivity. This conserved functional interaction enhances the steady-state levels of Vif proteins from multiple HIV-1 subtypes and is required for the degradation of all human and rhesus Vif-sensitive APOBEC3 proteins by their respective lentiviral Vif proteins.
引用
收藏
页码：2874 / 2877
页数：4
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