Abstract
HIV-1 requires the cellular transcription factor CBFβ to stabilize its accessory protein Vif and promote APOBEC3G degradation. Here, we demonstrate that both isoforms of CBFβ 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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Animals
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Core Binding Factor beta Subunit / genetics
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Core Binding Factor beta Subunit / metabolism*
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Cytidine Deaminase / genetics
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Cytidine Deaminase / metabolism*
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Gene Products, vif / chemistry
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Gene Products, vif / genetics
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Gene Products, vif / metabolism*
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HIV Infections / enzymology
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HIV Infections / genetics
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HIV Infections / metabolism*
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HIV Infections / virology
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HIV-1 / chemistry
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HIV-1 / genetics
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HIV-1 / metabolism*
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Humans
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Macaca mulatta
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Protein Isoforms / genetics
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Protein Isoforms / metabolism
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Protein Stability
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Simian Acquired Immunodeficiency Syndrome / enzymology
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Simian Acquired Immunodeficiency Syndrome / genetics
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Simian Acquired Immunodeficiency Syndrome / metabolism*
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Simian Acquired Immunodeficiency Syndrome / virology
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Simian Immunodeficiency Virus / chemistry
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Simian Immunodeficiency Virus / genetics
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Simian Immunodeficiency Virus / metabolism*
Substances
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Core Binding Factor beta Subunit
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Gene Products, vif
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Protein Isoforms
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Cytidine Deaminase