ArticleMolecular cell2013
CBFβ stabilizes HIV Vif to counteract APOBEC3 at the expense of RUNX1 target gene expression.
Article in Molecular cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
What it found
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Who cites it
87 citing papers in PubMed, 120 citations in OpenAlex.
- The structural mechanism of HIV-2 Vif antagonism of human APOBEC3H.Nature communications · 2026Article
- VHL synthetic lethality screens uncover CBF-β as a negative regulator of STING.Nature communications · 2026Article
- TARDBP as a regulator of HIV-1 assembly and infection: a review of targeting the viral capsid precursor Pr55Gag and limiting viral core entry.Cell communication and signaling : CCS · 2026Review
- HIV-1 vif mediates ubiquitination of the proximal protomer in the APOBEC3H dimer to induce degradation.Nature communications · 2025Article
- Article
- APOBEC3-Related Editing and Non-Editing Determinants of HIV-1 and HTLV-1 Restriction.International journal of molecular sciences · 2025Review
- Review
- Article
- Design of Vif-Derived Peptide Inhibitors with Anti-HIV-1 Activity by Interrupting Vif-CBFβ Interaction.Viruses · 2024Article
- Direct inhibition of human APOBEC3 deaminases by HIV-1 Vif independent of the proteolysis pathway.Biophysical journal · 2024Article
- Neddylation of protein, a new strategy of protein post-translational modification for targeted treatment of central nervous system diseases.Frontiers in neuroscience · 2024Review
- mRNA expression profile reveals differentially expressed genes in splenocytes of experimental autoimmune encephalomyelitis model.International journal of experimental pathology · 2023Article
- Review
- Dominant Negative Mutants of Human Immunodeficiency Virus Type 1 Viral Infectivity Factor (Vif) Disrupt Core-Binding Factor Beta-Vif Interaction.Journal of virology · 2022Article
- HIV-1 VIF and human APOBEC3G interaction directly observed through molecular specific labeling using a new dual promotor vector.Journal of magnetic resonance (San Diego, Calif. : 1997) · 2022Article
- Global post-translational modification profiling of HIV-1-infected cells reveals mechanisms of host cellular pathway remodeling.Cell reports · 2022Article
- Emerging role of protein modification in inflammatory bowel disease.Journal of Zhejiang University. Science. B · 2022Review
- RUNX1 inhibits the antiviral immune response against influenza A virus through attenuating type I interferon signaling.Virology journal · 2022Article
- HIV-1 Accessory Proteins Impart a Modest Interferon Response and Upregulate Cell Cycle-Related Genes in Macrophages.Pathogens (Basel, Switzerland) · 2022Article
- A Conserved uORF Regulates APOBEC3G Translation and Is Targeted by HIV-1 Vif Protein to Repress the Antiviral Factor.Biomedicines · 2021Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The HIV-1 accessory protein Vif hijacks a cellular Cullin-RING ubiquitin ligase, CRL5, to promote degradation of the APOBEC3 (A3) family of restriction factors. Recently, the cellular transcription cofactor CBFβ was shown to form a complex with CRL5-Vif and to be essential for A3 degradation and viral infectivity. We now demonstrate that CBFβ is required for assembling a well-ordered CRL5-Vif complex by inhibiting Vif oligomerization and by activating CRL5-Vif via direct interaction. The CRL5-Vif-CBFβ holoenzyme forms a well-defined heterohexamer, indicating that Vif simultaneously hijacks CRL5 and CBFβ. Heterodimers of CBFβ and RUNX transcription factors contribute toward the regulation of genes, including those with immune system functions. We show that binding of Vif to CBFβ is mutually exclusive with RUNX heterodimerization and impacts the expression of genes whose regulatory domains are associated with RUNX1. Our results provide a mechanism by which a pathogen with limited coding capacity uses one factor to hijack multiple host pathways.
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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.