ArticleCell cycle (Georgetown, Tex.)2013
Subcellular localization of the APOBEC3 proteins during mitosis and implications for genomic DNA deamination.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 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
106 citing papers in PubMed, 155 citations in OpenAlex.
- Structure of full-length APOBEC3B bound to EBV BORF2 reveals coordinated neutralization of a cancer-associated mutator.Research square · 2026Article
- Distinct repair processes produce APOBEC-induced deletions, tandem substitutions, and complex mutations in yeast and human cells.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- Squamous-state excursions activate APOBEC3A in cancer.bioRxiv : the preprint server for biology · 2026Article
- RNA editing: an emerging frontier in cancer therapy - explorations, opportunities, and challenges.International journal of surgery (London, England) · 2026Article
- Reprogramming tumor immunity through APOBEC3s-mediated mutagenesis: from genome instability to immune checkpoint interactions.Frontiers in immunology · 2026Review
- APOBEC3 promotes squamous differentiation via IL-1A/AP-1 signaling.Nature communications · 2025Article
- RNase H-sensitive accumulation of APOBEC3B in a nucleolus after DNA damage.Bioscience reports · 2025Article
- Regulatory Interactions between APOBEC3B N- and C-Terminal Domains.Journal of chemical information and modeling · 2025Article
- APOBEC3-Related Editing and Non-Editing Determinants of HIV-1 and HTLV-1 Restriction.International journal of molecular sciences · 2025Review
- An in vitro cytidine deaminase assay to monitor APOBEC activity on DNA.Methods in enzymology · 2025Article
- APOBEC3B expression in 293T viral producer cells drives mutations in chimeric antigen receptors and reduces CAR T cell efficacy.Molecular therapy. Oncology · 2024Article
- Regulatory interactions between APOBEC3B N- and C-terminal domains.bioRxiv : the preprint server for biology · 2024Article
- The cytidine deaminase APOBEC3A regulates nucleolar function to promote cell growth and ribosome biogenesis.PLoS biology · 2024Article
- Cytidine deaminases APOBEC3C and APOBEC3D promote DNA replication stress resistance in pancreatic cancer cells.Nature cancer · 2024Article
- Viral infection, APOBEC3 dysregulation, and cancer.Frontiers in genetics · 2024Review
- Monitoring APOBEC3A protein levels in human cancer cells.Methods in cell biology · 2024Article
- Engineered deaminases as a key component of DNA and RNA editing tools.Molecular therapy. Nucleic acids · 2023Review
- Acute expression of human APOBEC3B in mice results in RNA editing and lethality.Genome biology · 2023Article
- Mutational impact of APOBEC3A and APOBEC3B in a human cell line and comparisons to breast cancer.PLoS genetics · 2023Article
46 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 3 countries.
Funding
Abstract
Humans have seven APOBEC3 DNA cytosine deaminases. The activity of these enzymes allows them to restrict a variety of retroviruses and retrotransposons, but may also cause pro-mutagenic genomic uracil lesions. During interphase the APOBEC3 proteins have different subcellular localizations: cell-wide, cytoplasmic or nuclear. This implies that only a subset of APOBEC3s have contact with nuclear DNA. However, during mitosis, the nuclear envelope breaks down and cytoplasmic proteins may enter what was formerly a privileged zone. To address the hypothesis that all APOBEC3 proteins have access to genomic DNA, we analyzed the localization of the APOBEC3 proteins during mitosis. We show that APOBEC3A, APOBEC3C and APOBEC3H are excluded from condensed chromosomes, but become cell-wide during telophase. However, APOBEC3B, APOBEC3D, APOBEC3F and APOBEC3G are excluded from chromatin throughout mitosis. After mitosis, APOBEC3B becomes nuclear, and APOBEC3D, APOBEC3F and APOBEC3G become cytoplasmic. Both structural motifs as well as size may be factors in regulating chromatin exclusion. Deaminase activity was not dependent on cell cycle phase. We also analyzed APOBEC3-induced cell cycle perturbations as a measure of each enzyme's capacity to inflict genomic DNA damage. AID, APOBEC3A and APOBEC3B altered the cell cycle profile, and, unexpectedly, APOBEC3D also caused changes. We conclude that several APOBEC3 family members have access to the nuclear compartment and can impede the cell cycle, most likely through DNA deamination and the ensuing DNA damage response. Such genomic damage may contribute to carcinogenesis, as demonstrated by AID in B cell cancers and, recently, APOBEC3B in breast cancers.
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.