ArticleJournal of virology2008
Interactions of murine APOBEC3 and human APOBEC3G with murine leukemia viruses.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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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.
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
58 citing papers in PubMed, 78 citations in OpenAlex.
- A Viral Protein Antagonist for Both AID and APOBEC3.Viruses · 2026Review
- MMTV-like Viruses and Human Breast Cancer: Evidence for Causality.Current issues in molecular biology · 2026Review
- Article
- DHX15 inhibits mouse APOBEC3 deamination.PLoS pathogens · 2025Article
- Essential functions of inositol hexakisphosphate (IP6) in murine leukemia virus replication.mBio · 2024Article
- Repair of APOBEC3G-Mutated Retroviral DNAJournal of virology · 2021Article
- Deaminase-Independent Mode of Antiretroviral Action in Human and Mouse APOBEC3 Proteins.Microorganisms · 2020Review
- Retroviral Restriction Factors and Their Viral Targets: Restriction Strategies and Evolutionary Adaptations.Microorganisms · 2020Review
- The Role of APOBECs in Viral Replication.Microorganisms · 2020Review
- Mouse APOBEC3 Restriction of Retroviruses.Viruses · 2020Review
- Mouse APOBEC3 interferes with autocatalytic cleavage of murine leukemia virus Pr180gag-pol precursor and inhibits Pr65gag processing.PLoS pathogens · 2019Article
- DNA Adsorption Studies of Poly(4,4'-Cychlohexylidene Bisphenol Oxalate)/Silica Nanocomposites.Materials (Basel, Switzerland) · 2019Article
- Deaminase-Dead Mouse APOBEC3 Is anJournal of virology · 2018Article
- Asymmetric Modification of Hepatitis B Virus (HBV) Genomes by an Endogenous Cytidine Deaminase inside HBV Cores Informs a Model of Reverse Transcription.Journal of virology · 2018Article
- The cytidine deaminase under-representation reporter (CDUR) as a tool to study evolution of sequences under deaminase mutational pressure.BMC bioinformatics · 2018Article
- Mouse APOBEC3 expression in NIH 3T3 cells mediates hypermutation of AKV murine leukemia virus.Virology · 2018Article
- Full-Length Glycosylated Gag of Murine Leukemia Virus Can Associate with the Viral Envelope as a Type I Integral Membrane Protein.Journal of virology · 2018Article
- The preferred nucleotide contexts of the AID/APOBEC cytidine deaminases have differential effects when mutating retrotransposon and virus sequences compared to host genes.PLoS computational biology · 2017Article
- Current Nucleic Acid Extraction Methods and Their Implications to Point-of-Care Diagnostics.BioMed research international · 2017Review
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
APOBEC3 proteins are cytidine deaminases which help defend cells against retroviral infections. One antiviral mechanism involves deaminating dC residues in minus-strand DNA during reverse transcription, resulting in G-to-A mutations in the coding strand. We investigated the effects of mouse APOBEC3 (mA3) and human APOBEC3G (hA3G) upon Moloney murine leukemia virus (MLV). We find that mA3 inactivates MLV but is significantly less effective against MLV than is hA3G. In contrast, mA3 is as potent against human immunodeficiency virus type 1 (HIV-1, lacking the protective Vif protein) as is hA3G. The two APOBEC3 proteins are packaged to similar extents in MLV particles. Dose-response profiles imply that a single APOBEC3 molecule (or oligomer) is sufficient to inactivate an MLV particle. The inactivation of MLV by mA3 and hA3G is accompanied by relatively small reductions in the amount of viral DNA in infected cells. Although hA3G induces significant levels of G-to-A mutations in both MLV and HIV DNAs, and mA3 induces these mutations in HIV DNA, no such mutations were detected in DNA synthesized by MLV inactivated by mA3. Thus, MLV has apparently evolved to partially resist the antiviral effects of mA3 and to totally resist the ability of mA3 to induce G-to-A mutation in viral DNA. Unlike the resistance of HIV-1 and human T-cell leukemia virus type 1 to hA3G, the resistance of MLV to mA3 is not mediated by the exclusion of APOBEC from the virus particle. The nature of its resistance and the mechanism of inactivation of MLV by mA3 are completely unknown.
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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.