ArticleRetrovirology2013
Interactions between HIV-1 Vif and human ElonginB-ElonginC are important for CBF-β binding to Vif.
Article in Retrovirology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- Tree Shrew Cells Transduced with Human CD4 and CCR5 Support Early Steps of HIV-1 Replication, but Viral Infectivity Is Restricted by APOBEC3.Journal of virology · 2021Article
- Inhibition of Vif-Mediated Degradation of APOBEC3G through Competitive Binding of Core-Binding Factor Beta.Journal of virology · 2020Article
- Immunoproteomic and mass spectrometric analysis of Eimeria acervulina antigens recognized by antisera from chickens infected with E. acervulina, E. tenella or E. necatrix.Parasites & vectors · 2020Article
- Moloney leukemia virus 10 (MOV10) inhibits the degradation of APOBEC3G through interference with the Vif-mediated ubiquitin-proteasome pathway.Retrovirology · 2017Article
- Clues for two-step virion infectivity factor regulation by core binding factor beta.The Journal of general virology · 2017Article
- Article
- The HDAC6/APOBEC3G complex regulates HIV-1 infectiveness by inducing Vif autophagic degradation.Retrovirology · 2015Article
- The Road Less Traveled: HIV's Use of Alternative Routes through Cellular Pathways.Journal of virology · 2015Review
- Identification of a novel HIV-1 inhibitor targeting Vif-dependent degradation of human APOBEC3G protein.The Journal of biological chemistry · 2015Article
- Determinants of efficient degradation of APOBEC3 restriction factors by HIV-1 Vif.Journal of virology · 2014Article
- Requirement of HIV-1 Vif C-terminus for Vif-CBF-β interaction and assembly of CUL5-containing E3 ligase.BMC microbiology · 2014Article
- Role of cullin-elonginB-elonginC E3 complex in bovine immunodeficiency virus and maedi-visna virus Vif-mediated degradation of host A3Z2-Z3 proteins.Retrovirology · 2014Article
- Article
- HIV-1 Vif N-terminal motif is required for recruitment of Cul5 to suppress APOBEC3.Retrovirology · 2014Article
- Suppression of APOBEC3-mediated restriction of HIV-1 by Vif.Frontiers in microbiology · 2014Review
- Identification of HIV-1 Vif regions required for CBF-β interaction and APOBEC3 suppression.PloS one · 2014Article
- Structural analysis of viral infectivity factor of HIV type 1 and its interaction with A3G, EloC and EloB.PloS one · 2014Article
- Insight into the HIV-1 Vif SOCS-box-ElonginBC interaction.Open biology · 2013Article
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe HIV-1 accessory factor Vif is necessary for efficient viral infection in non-permissive cells. Vif antagonizes the antiviral activity of human cytidine deaminase APOBEC3 proteins that confer the non-permissive phenotype by tethering them (APOBEC3DE/3F/3G) to the Vif-CBF-β-ElonginB-ElonginC-Cullin5-Rbx (Vif-CBF-β-EloB-EloC-Cul5-Rbx) E3 complex to induce their proteasomal degradation. EloB and EloC were initially reported as positive regulatory subunits of the Elongin (SIII) complex. Thereafter, EloB and EloC were found to be components of Cul-E3 complexes, contributing to proteasomal degradation of specific substrates. CBF-β is a newly identified key regulator of Vif function, and more information is needed to further clarify its regulatory mechanism. Here, we comprehensively investigated the functions of EloB (together with EloC) in the Vif-CBF-β-Cul5 E3 ligase complex.
resultsThe results revealed that: (1) EloB (and EloC) positively affected the recruitment of CBF-β to Vif. Both knockdown of endogenous EloB and over-expression of its mutant with a 34-residue deletion in the COOH-terminal tail (EloBΔC34/EBΔC34) impaired the Vif-CBF-β interaction. (2) Introduction of both the Vif SLQ → AAA mutant (VifΔSLQ, which dramatically impairs Vif-EloB-EloC binding) and the Vif PPL → AAA mutant (VifΔPPL, which is thought to reduce Vif-EloB binding) could reduce CBF-β binding. (3) EloB-EloC but not CBF-β could greatly enhance the folding of full-length Vif in Escherichia coli. (4) The over-expression of EloB or the N-terminal ubiquitin-like (UbL) domain of EloB could significantly improve the stability of Vif/VifΔSLQ/VifΔPPL through the region between residues 9 and 14.
conclusionOur results indicate that the Vif interaction with EloB-EloC may contribute to recruitment of CBF-β to Vif, demonstrating that the EloB C-teminus may play a role in improving Vif function and that the over-expression of EloB results in Vif stabilization.
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