ArticleCell reports2019
HIV-1 Vif Triggers Cell Cycle Arrest by Degrading Cellular PPP2R5 Phospho-regulators.
Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed.
- Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026Review
- Strain-specific epistasis shapes fitness landscapes of APOBEC3G antagonism by HIV-1 Vif proteins.Science advances · 2026Article
- PPP2R5B regulates ANPEP expression and TGEV entry via dephosphorylation of HSF1 at Ser304/Ser308.Journal of virology · 2026Article
- Review
- Article
- DNA damage induced by HIV-1 Vpr triggers epigenetic remodeling and transcriptional programs to enhance virus transcription and latency reactivation.PLoS biology · 2026Article
- HIV-1 Vif and Vpr cooperatively modulate the cell cycle to maximize per-cell virion production.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Fitness Landscapes of APOBEC3G Antagonism by HIV-1 Vif proteins.bioRxiv : the preprint server for biology · 2025Article
- APOBEC3G Antagonism by Vif, or When Structure Meets Biological and Evolutionary Studies.Annual review of virology · 2025Review
- Single-cell delineation of strain-specific HIV-1 Vif activities using dual reporter sensor cells and live cell imaging.Journal of virology · 2025Article
- Article
- Article
- APOBEC3-Related Editing and Non-Editing Determinants of HIV-1 and HTLV-1 Restriction.International journal of molecular sciences · 2025Review
- HIV-1 Vif disrupts phosphatase feedback regulation at the kinetochore, leading to a pronounced pseudo-metaphase arrest.bioRxiv : the preprint server for biology · 2024Article
- Structural insights into PPP2R5A degradation by HIV-1 Vif.Nature structural & molecular biology · 2024Article
- The association between HIV-1 Tat and Vif amino acid sequence variation, inflammation and Trp-Kyn metabolism: an exploratory investigation.BMC infectious diseases · 2024Article
- HIV-1 Vif protein sequence variations in South African people living with HIV and their influence on Vif-APOBEC3G interaction.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2024Article
- Inhibition of ATM-directed antiviral responses by HIV-1 Vif.PLoS pathogens · 2023Article
- Article
- APOBEC3 degradation is the primary function of HIV-1 Vif for virus replication in the myeloid cell line THP-1.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
HIV-1 Vif hijacks a cellular ubiquitin ligase complex to degrade antiviral APOBEC3 enzymes and PP2A phosphatase regulators (PPP2R5A-E). APOBEC3 counteraction is essential for viral pathogenesis. However, Vif also functions through an unknown mechanism to induce G2 cell cycle arrest. Here, deep mutagenesis is used to define the Vif surface required for PPP2R5 degradation and isolate a panel of separation-of-function mutants (PPP2R5 degradation-deficient and APOBEC3G degradation-proficient). Functional studies with Vif and PPP2R5 mutants were combined to demonstrate that PPP2R5 is, in fact, the target Vif degrades to induce G2 arrest. Pharmacologic and genetic approaches show that direct modulation of PP2A function or depletion of specific PPP2R5 proteins causes an indistinguishable arrest phenotype. Vif function in the cell cycle checkpoint is present in common HIV-1 subtypes worldwide and likely advantageous for viral pathogenesis.
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.