ArticleJournal of virology2011
Identification of a Cullin5-ElonginB-ElonginC E3 complex in degradation of feline immunodeficiency virus Vif-mediated feline APOBEC3 proteins.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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.
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Who cites it
24 citing papers in PubMed, 31 citations in OpenAlex.
- A Cullin 5-based complex serves as an essential modulator of ORF9b stability in SARS-CoV-2 replication.Signal transduction and targeted therapy · 2024Article
- Antiviral Activity of Feline BCA2 Is Mainly Dependent on Its Interference With Proviral Transcription Rather Than Degradation of FIV Gag.Frontiers in microbiology · 2020Article
- Article
- CAEV Vif Hijacks ElonginB/C, CYPA and Cullin5 to Assemble the E3 Ubiquitin Ligase Complex Stepwise to Degrade oaA3Z2-Z3.Frontiers in microbiology · 2019Article
- Replacement of feline foamy virus bet by feline immunodeficiency virus vif yields replicative virus with novel vaccine candidate potential.Retrovirology · 2018Article
- New World feline APOBEC3 potently controls inter-genus lentiviral transmission.Retrovirology · 2018Article
- Review
- Identification of a Conserved Interface of Human Immunodeficiency Virus Type 1 and Feline Immunodeficiency Virus Vifs with Cullin 5.Journal of virology · 2018Article
- Moloney leukemia virus 10 (MOV10) inhibits the degradation of APOBEC3G through interference with the Vif-mediated ubiquitin-proteasome pathway.Retrovirology · 2017Article
- Feline Immunodeficiency Virus Evolutionarily Acquires Two Proteins, Vif and Protease, Capable of Antagonizing Feline APOBEC3.Journal of virology · 2017Article
- A conflict of interest: the evolutionary arms race between mammalian APOBEC3 and lentiviral Vif.Retrovirology · 2017Review
- Feline Immunodeficiency Virus Vif N-Terminal Residues Selectively Counteract Feline APOBEC3s.Journal of virology · 2016Article
- Determinants of FIV and HIV Vif sensitivity of feline APOBEC3 restriction factors.Retrovirology · 2016Article
- The effect of HIV-1 Vif polymorphisms on A3G anti-viral activity in an in vivo mouse model.Retrovirology · 2016Article
- Article
- Degradation of the cancer genomic DNA deaminase APOBEC3B by SIV Vif.Oncotarget · 2015Article
- The Road Less Traveled: HIV's Use of Alternative Routes through Cellular Pathways.Journal of virology · 2015Review
- Vif determines the requirement for CBF-β in APOBEC3 degradation.The Journal of general virology · 2015Article
- Viral Restriction Activity of Feline BST2 Is Independent of Its N-Glycosylation and Induction of NF-κB Activation.PloS one · 2015Article
- Core-binding factor subunit beta is not required for non-primate lentiviral Vif-mediated APOBEC3 degradation.Journal of virology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Various feline APOBEC3 (fA3) proteins exhibit broad antiviral activities against a wide range of viruses, such as feline immunodeficiency virus (FIV), feline foamy virus (FFV), and feline leukemia virus (FeLV), as well as those of other species. This activity can be counteracted by the FIV Vif protein, but the mechanism by which FIV Vif suppresses fA3s is unknown. In the present study, we demonstrated that FIV Vif could act via a proteasome-dependent pathway to overcome fA3s. FIV Vif interacted with feline cellular proteins Cullin5 (Cul5), ElonginB, and ElonginC to form an E3 complex to induce degradation of fA3s. Both the dominant-negative Cul5 mutant and a C-terminal hydrophilic replacement ElonginC mutant potently disrupted the FIV Vif activity against fA3s. Furthermore, we identified a BC-box motif in FIV Vif that was essential for the recruitment of E3 ubiquitin ligase and also required for FIV Vif-mediated degradation of fA3s. Moreover, despite the lack of either a Cul5-box or a HCCH zinc-binding motif, FIV Vif specifically selected Cul5. Therefore, FIV Vif may interact with Cul5 via a novel mechanism. These finding imply that SOCS proteins may possess distinct mechanisms to bind Cul5 during formation of the Elongin-Cullin-SOCS box complex.
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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.