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

页码：2874 / 2877

页数：4

共 13 条

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