ArticlePLoS pathogens2010
The SOCS-box of HIV-1 Vif interacts with ElonginBC by induced-folding to recruit its Cul5-containing ubiquitin ligase complex.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 83 citations in OpenAlex.
- Suppressor of cytokine signaling (SOCS) proteins in human retroviral infections.Molecular biology reports · 2026Review
- Mechanisms of Immune Evasion in HIV-1: The Role of Virus-Host Protein Interactions.Current issues in molecular biology · 2025Review
- Genetic Signatures of Positive Selection in Human Populations Adapted to High Altitude in Papua New Guinea.Genome biology and evolution · 2024Article
- Dominant Negative Mutants of Human Immunodeficiency Virus Type 1 Viral Infectivity Factor (Vif) Disrupt Core-Binding Factor Beta-Vif Interaction.Journal of virology · 2022Article
- A Conserved uORF Regulates APOBEC3G Translation and Is Targeted by HIV-1 Vif Protein to Repress the Antiviral Factor.Biomedicines · 2021Article
- Examination of the APOBEC3 Barrier to Cross Species Transmission of Primate Lentiviruses.Viruses · 2021Review
- Characterization of an A3G-VifMolecular & cellular proteomics : MCP · 2021Article
- High-speed atomic force microscopy directly visualizes conformational dynamics of the HIV Vif protein in complex with three host proteins.The Journal of biological chemistry · 2020Article
- Structural perspectives on HIV-1 Vif and APOBEC3 restriction factor interactions.Protein science : a publication of the Protein Society · 2020Review
- Dual Functionality of HIV-1 Vif in APOBEC3 Counteraction and Cell Cycle Arrest.Frontiers in microbiology · 2020Review
- Article
- Article
- A New Class of Antiretroviral Enabling Innate Immunity by Protecting APOBEC3 from HIV Vif-Dependent Degradation.Trends in molecular medicine · 2018Review
- HIV-1 Vif's Capacity To Manipulate the Cell Cycle Is Species Specific.Journal of virology · 2018Article
- Identification of a Conserved Interface of Human Immunodeficiency Virus Type 1 and Feline Immunodeficiency Virus Vifs with Cullin 5.Journal of virology · 2018Article
- Control of HIV infection by IFN-α: implications for latency and a cure.Cellular and molecular life sciences : CMLS · 2018Review
- Moloney leukemia virus 10 (MOV10) inhibits the degradation of APOBEC3G through interference with the Vif-mediated ubiquitin-proteasome pathway.Retrovirology · 2017Article
- Immune regulator ABIN1 suppresses HIV-1 transcription by negatively regulating the ubiquitination of Tat.Retrovirology · 2017Article
- Are Evolution and the Intracellular Innate Immune System Key Determinants in HIV Transmission?Frontiers in immunology · 2017Review
- An analog of camptothecin inactive against Topoisomerase I is broadly neutralizing of HIV-1 through inhibition of Vif-dependent APOBEC3G degradation.Antiviral research · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The HIV-1 viral infectivity factor (Vif) protein recruits an E3 ubiquitin ligase complex, comprising the cellular proteins elongin B and C (EloBC), cullin 5 (Cul5) and RING-box 2 (Rbx2), to the anti-viral proteins APOBEC3G (A3G) and APOBEC3F (A3F) and induces their polyubiquitination and proteasomal degradation. In this study, we used purified proteins and direct in vitro binding assays, isothermal titration calorimetry and NMR spectroscopy to describe the molecular mechanism for assembly of the Vif-EloBC ternary complex. We demonstrate that Vif binds to EloBC in two locations, and that both interactions induce structural changes in the SOCS box of Vif as well as EloBC. In particular, in addition to the previously established binding of Vif's BC box to EloC, we report a novel interaction between the conserved Pro-Pro-Leu-Pro motif of Vif and the C-terminal domain of EloB. Using cell-based assays, we further show that this interaction is necessary for the formation of a functional ligase complex, thus establishing a role of this motif. We conclude that HIV-1 Vif engages EloBC via an induced-folding mechanism that does not require additional co-factors, and speculate that these features distinguish Vif from other EloBC specificity factors such as cellular SOCS proteins, and may enhance the prospects of obtaining therapeutic inhibitors of Vif function.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.