ArticleJournal of virology2010
Identification of a critical T(Q/D/E)x5ADx2(I/L) motif from primate lentivirus Vif proteins that regulate APOBEC3G and APOBEC3F neutralizing activity.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- HIV Genome-Wide Protein Associations: a Review of 30 Years of Research.Microbiology and molecular biology reviews : MMBR · 2016Pooled it
- Strain-specific epistasis shapes fitness landscapes of APOBEC3G antagonism by HIV-1 Vif proteins.Science advances · 2026Article
- Suppressor of cytokine signaling (SOCS) proteins in human retroviral infections.Molecular biology reports · 2026Review
- Fitness Landscapes of APOBEC3G Antagonism by HIV-1 Vif proteins.bioRxiv : the preprint server for biology · 2025Article
- Multifaceted HIV-1 Vif interactions with human E3 ubiquitin ligase and APOBEC3s.The FEBS journal · 2021Article
- Characterization of an A3G-VifMolecular & cellular proteomics : MCP · 2021Article
- Review
- Structural perspectives on HIV-1 Vif and APOBEC3 restriction factor interactions.Protein science : a publication of the Protein Society · 2020Review
- Feline Immunodeficiency Virus Vif N-Terminal Residues Selectively Counteract Feline APOBEC3s.Journal of virology · 2016Article
- Vif Proteins from Diverse Human Immunodeficiency Virus/Simian Immunodeficiency Virus Lineages Have Distinct Binding Sites in A3C.Journal of virology · 2016Article
- Role of the single deaminase domain APOBEC3A in virus restriction, retrotransposition, DNA damage and cancer.The Journal of general virology · 2016Review
- Article
- Anti-APOBEC3G activity of HIV-1 Vif protein is attenuated in elite controllers.Journal of virology · 2015Article
- Identification of a novel HIV-1 inhibitor targeting Vif-dependent degradation of human APOBEC3G protein.The Journal of biological chemistry · 2015Article
- Requirement of HIV-1 Vif C-terminus for Vif-CBF-β interaction and assembly of CUL5-containing E3 ligase.BMC microbiology · 2014Article
- Core-binding factor subunit beta is not required for non-primate lentiviral Vif-mediated APOBEC3 degradation.Journal of virology · 2014Article
- Structural insights for HIV-1 therapeutic strategies targeting Vif.Trends in biochemical sciences · 2014Review
- CBFβ enhances de novo protein biosynthesis of its binding partners HIV-1 Vif and RUNX1 and potentiates the Vif-induced degradation of APOBEC3G.Journal of virology · 2014Article
- Multiple APOBEC3 restriction factors for HIV-1 and one Vif to rule them all.Journal of molecular biology · 2014Review
- Core binding factor beta plays a critical role by facilitating the assembly of the Vif-cullin 5 E3 ubiquitin ligase.Journal of virology · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Primate lentiviruses are unique in that they produce several accessory proteins to help in the establishment of productive viral infection. The major function of these proteins is to clear host resistance factors that inhibit viral replication. Vif is one of these proteins. It functions as an adaptor that binds to the cytidine deaminases APOBEC3G (A3G) and APOBEC3F (A3F) and bridges them to a cullin 5 (Cul5) and elongin (Elo) B/C E3 ubiquitin ligase complex for proteasomal degradation. So far, 11 discontinuous domains in Vif have been identified that regulate this degradation process. Here we report another domain, T(Q/D/E)x(5)ADx(2)(I/L), which is located at residues 96 to 107 in the human immunodeficiency virus type 1 (HIV-1) Vif protein. This domain is conserved not only in all HIV-1 subtypes but also in other primate lentiviruses, including HIV-2 and simian immunodeficiency virus (SIV), which infects rhesus macaques (SIVmac) and African green monkeys (SIVagm). Mutations of the critical residues in this motif seriously disrupted Vif's neutralizing activity toward both A3G and A3F. This motif regulates Vif interaction not only with A3G and A3F but also with Cul5. When this motif was inactivated in the HIV-1 genome, Vif failed to exclude A3G and A3F from virions, resulting in abortive HIV replication in nonpermissive human T cells. Thus, T(Q/D/E)x(5)ADx(2)(I/L) is a critical functional motif that directly supports the adaptor function of Vif and is an attractive target for inhibition of Vif function.
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