ArticleTrends in biochemical sciences2011
APOBEC3G: a double agent in defense.
Article in Trends in biochemical sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Evolutionary Comparative Analyses of DNA-Editing Enzymes of the Immune System: From 5-Dimensional Description of Protein Structures to Immunological Insights and Applications to Protein Engineering.Frontiers in immunology · 2021Pooled it
- RNA editing: an emerging frontier in cancer therapy - explorations, opportunities, and challenges.International journal of surgery (London, England) · 2026Article
- The mutational landscape of SARS-CoV-2 provides new insight into viral evolution and fitness.Nature communications · 2025Article
- Structure-Based Design of First-Generation Small Molecule Inhibitors Targeting the Catalytic Pockets of AID, APOBEC3A, and APOBEC3B.ACS pharmacology & translational science · 2021Article
- Review
- DNA mutagenic activity and capacity for HIV-1 restriction of the cytidine deaminase APOBEC3G depend on whether DNA or RNA binds to tyrosine 315.The Journal of biological chemistry · 2017Article
- A putative antiviral role of plant cytidine deaminases.F1000Research · 2017Article
- APOBEC3B, a molecular driver of mutagenesis in human cancers.Cell & bioscience · 2017Review
- Structural and functional assessment of APOBEC3G macromolecular complexes.Methods (San Diego, Calif.) · 2016Article
- The APOBEC Protein Family: United by Structure, Divergent in Function.Trends in biochemical sciences · 2016Review
- Associations between activation-induced cytidine deaminase/apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like cytidine deaminase expression, hepatitis B virus (HBV) replication and HBV-associated liver disease (Review).Molecular medicine reports · 2015Review
- RNA binding to APOBEC3G induces the disassembly of functional deaminase complexes by displacing single-stranded DNA substrates.Nucleic acids research · 2015Article
- The virus-induced protein APOBEC3G inhibits anoikis by activation of Akt kinase in pancreatic cancer cells.Scientific reports · 2015Article
- The HDAC6/APOBEC3G complex regulates HIV-1 infectiveness by inducing Vif autophagic degradation.Retrovirology · 2015Article
- Positioning of APOBEC3G/F mutational hotspots in the human immunodeficiency virus genome favors reduced recognition by CD8+ T cells.PloS one · 2014Article
- GANP interacts with APOBEC3G and facilitates its encapsidation into the virions to reduce HIV-1 infectivity.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Host Factors and HIV-1 Replication: Clinical Evidence and Potential Therapeutic Approaches.Frontiers in immunology · 2013Review
- APOBEC3G-Augmented Stem Cell Therapy to Modulate HIV Replication: A Computational Study.PloS one · 2013Article
- Lower HIV provirus levels are associated with more APOBEC3G protein in blood resting memory CD4+ T lymphocytes of controllers in vivo.PloS one · 2013Article
- Host restriction factors in retroviral infection: promises in virus-host interaction.Retrovirology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
APOBEC3G (A3G) is an effective cellular host defense factor under experimental conditions in which a functional form of the HIV-encoded protein Vif cannot be expressed. Wild-type Vif targets A3G for proteasomal degradation and when this happens, any host defense advantage A3G might provide is severely diminished or lost. Recent evidence cast doubt on the potency of A3G in host defense and suggested that it could, under some circumstances, promote the emergence of more virulent HIV strains. In this article, I suggest that it is time to recognize that A3G has the potential to act as a double agent. Future research should focus on understanding how cellular and viral regulatory mechanisms enable the antiviral function of A3G, and on the development of novel research reagents to explore these pathways.
Indexed as
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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.