ArticlePLoS pathogens2007
T cells contain an RNase-insensitive inhibitor of APOBEC3G deaminase activity.
Article in PLoS pathogens, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 48 citations in OpenAlex.
- APOBEC3B Does Not Promote Tumor Progression in Tp53 Hemizygous Mice.Cancer reports (Hoboken, N.J.) · 2025Article
- The current toolbox for APOBEC drug discovery.Trends in pharmacological sciences · 2022Review
- The endoplasmic reticulum proteostasis network profoundly shapes the protein sequence space accessible to HIV envelope.PLoS biology · 2022Article
- Article
- Deamination hotspots among APOBEC3 family members are defined by both target site sequence context and ssDNA secondary structure.Nucleic acids research · 2020Article
- A Rabbit Monoclonal Antibody against the Antiviral and Cancer Genomic DNA Mutating Enzyme APOBEC3B.Antibodies (Basel, Switzerland) · 2019Article
- Protein kinase A inhibits tumor mutator APOBEC3B through phosphorylation.Scientific reports · 2019Article
- The Antiviral and Cancer Genomic DNA Deaminase APOBEC3H Is Regulated by an RNA-Mediated Dimerization Mechanism.Molecular cell · 2018Article
- APOBEC3A Is Upregulated by Human Cytomegalovirus (HCMV) in the Maternal-Fetal Interface, Acting as an Innate Anti-HCMV Effector.Journal of virology · 2017Article
- HIV-1 Vif inhibits G to A hypermutations catalyzed by virus-encapsidated APOBEC3G to maintain HIV-1 infectivity.Retrovirology · 2014Article
- Article
- The local dinucleotide preference of APOBEC3G can be altered from 5'-CC to 5'-TC by a single amino acid substitution.Journal of molecular biology · 2013Article
- APOBEC3G cytosine deamination hotspots are defined by both sequence context and single-stranded DNA secondary structure.Nucleic acids research · 2013Article
- Impact of H216 on the DNA binding and catalytic activities of the HIV restriction factor APOBEC3G.Journal of virology · 2013Article
- APOBEC3G-Augmented Stem Cell Therapy to Modulate HIV Replication: A Computational Study.PloS one · 2013Article
- HIV-1 Gag co-opts a cellular complex containing DDX6, a helicase that facilitates capsid assembly.The Journal of cell biology · 2012Article
- First-in-class small molecule inhibitors of the single-strand DNA cytosine deaminase APOBEC3G.ACS chemical biology · 2012Article
- APOBEC3 versus Retroviruses, Immunity versus Invasion: Clash of the Titans.Molecular biology international · 2012Article
- An initial in vitro investigation into the potential therapeutic use of SupT1 cells to prevent AIDS in HIV-seropositive individuals.PloS one · 2012Article
- APOBEC3 proteins and genomic stability: the high cost of a good defense.Cell cycle (Georgetown, Tex.) · 2012Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The deoxycytidine deaminase APOBEC3G (A3G) is expressed in human T cells and inhibits HIV-1 replication. When transfected into A3G-deficient epithelial cell lines, A3G induces catastrophic hypermutation by deaminating the HIV-1 genome. Interestingly, studies suggest that endogenous A3G in T cells induces less hypermutation than would be expected. However, to date, the specific deaminase activity of endogenous A3G in human CD4+ T cells has not been examined directly. Here, we compared deaminase activity of endogenous and exogenous A3G in various human cell lines using a standard assay and a novel, quantitative, high-throughput assay. Exogenous A3G in epithelial cell lysates displayed deaminase activity only following RNase treatment, as expected given that A3G is known to form an enzymatically inactive RNA-containing complex. Surprisingly, comparable amounts of endogenous A3G from T cell lines or from resting or activated primary CD4+ T cells exhibited minimal deaminase activity, despite RNase treatment. Specific deaminase activity of endogenous A3G in H9, CEM, and other T cell lines was up to 36-fold lower than specific activity of exogenous A3G in epithelial-derived cell lines. Furthermore, RNase-treated T cell lysates conferred a dose-dependent inhibition to epithelial cell lysates expressing enzymatically active A3G. These studies suggest that T cells, unlike epithelial-derived cell lines, express an unidentified RNase-resistant factor that inhibits A3G deaminase activity. This factor could be responsible for reduced levels of hypermutation in T cells, and its identification and blockade could offer a means for increasing antiretroviral intrinsic immunity of T cells.
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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.