机构:
Mt Sinai Sch Med, Dept Microbiol, New York, NY USA
Mt Sinai Sch Med, Global Hlth & Emerging Pathogens Inst, New York, NY USA
Mt Sinai Sch Med, Dept Med, Div Infect Dis, New York, NY USAUniv Minnesota, Dept Biochem Mol Biol & Biophys, Inst Mol Virol, Ctr Genome Engn,Masonic Canc Ctr, Minneapolis, MN 55455 USA
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.
机构:
Univ Namur, Namur Res Inst Life Sci NARILIS, Integrated Vet Res Unit URVI, Namur, BelgiumUniv Namur, Namur Res Inst Life Sci NARILIS, Integrated Vet Res Unit URVI, Namur, Belgium
Poulain, Florian
Lejeune, Noemie
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Univ Namur, Namur Res Inst Life Sci NARILIS, Integrated Vet Res Unit URVI, Namur, BelgiumUniv Namur, Namur Res Inst Life Sci NARILIS, Integrated Vet Res Unit URVI, Namur, Belgium
Lejeune, Noemie
Willemart, Kevin
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Univ Namur, Namur Res Inst Life Sci NARILIS, Integrated Vet Res Unit URVI, Namur, BelgiumUniv Namur, Namur Res Inst Life Sci NARILIS, Integrated Vet Res Unit URVI, Namur, Belgium
Willemart, Kevin
Gillet, Nicolas A.
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Univ Namur, Namur Res Inst Life Sci NARILIS, Integrated Vet Res Unit URVI, Namur, BelgiumUniv Namur, Namur Res Inst Life Sci NARILIS, Integrated Vet Res Unit URVI, Namur, Belgium