Abstract
The Vif (viral infectivity factor) protein of human immunodeficiency virus type-1 (HIV-1) is critical for HIV-1 infectivity. CBF-β is required for HIV-1 Vif function, as it increases the steady-state level of the HIV-1 Vif protein to promote host restriction factor APOBEC3 degradation. However, the precise mechanism by which CBF-β promotes HIV-1 Vif levels remains unclear. In the present study, we provided evidences that CBF-β promoted steady-state levels of HIV-1 Vif by inhibiting the degradation of HIV-1 Vif through the proteasome pathway. Our results reveal a new mechanism by which a cellular protein supports viral infectivity by inhibiting viral protein degradation.
Keywords:
A3G; CBF-β; HIV-1; Proteasome pathway; Vif.
Copyright © 2015 Elsevier Inc. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Substitution
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Core Binding Factor beta Subunit / genetics
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Core Binding Factor beta Subunit / metabolism*
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HEK293 Cells
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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 / genetics
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HIV-1 / metabolism*
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HIV-1 / pathogenicity
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Host-Pathogen Interactions
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Humans
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Lysine / chemistry
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Mutagenesis, Site-Directed
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Proteasome Endopeptidase Complex / metabolism
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Proteolysis
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Recombinant Proteins / chemistry
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Recombinant Proteins / genetics
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Recombinant Proteins / metabolism
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Virulence
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vif Gene Products, Human Immunodeficiency Virus / chemistry*
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vif Gene Products, Human Immunodeficiency Virus / genetics
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vif Gene Products, Human Immunodeficiency Virus / metabolism*
Substances
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CBFB protein, human
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Core Binding Factor beta Subunit
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Recombinant Proteins
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vif Gene Products, Human Immunodeficiency Virus
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vif protein, Human immunodeficiency virus 1
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Proteasome Endopeptidase Complex
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Lysine