ArticleCell reports2016
APOBEC3A and APOBEC3B Preferentially Deaminate the Lagging Strand Template during DNA Replication.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 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
156 citing papers in PubMed, 228 citations in OpenAlex.
- Unraveling the lexicon of complex mutational phenomena in human cancers.Nature cancer · 2026Review
- APOBEC3 activity and DNA polymerase-ε deficiency are associated with distinct IDH1 R132 hotspot mutations.Molecular oncology · 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
- Click-code-seq reveals strand biases of DNA oxidation and depurination in human genome.Nature chemical biology · 2026Article
- Increased replication-associated single-stranded DNA promotes formaldehyde-induced mutagenesis.bioRxiv : the preprint server for biology · 2026Article
- Effects of thymidylate synthase inhibitors differ in genomic uracilation and mutagenic potential.Life science alliance · 2026Article
- R-loop editing by DNA cytosine deaminase APOBEC3B modulates the activity of oestrogen receptor enhancers.Nature communications · 2026Article
- Genomic Instability and Adaptive Evolution Induced by RFA Insufficiency inCurrent issues in molecular biology · 2026Article
- Hypoxia-mimicked mitochondrial stress triggers APOBEC3A-mediated DNA damage via non-canonical innate immune activation.NAR molecular medicine · 2026Article
- APOBEC3A-Induced DNA Damage Drives Polymerase θ Dependency and Synthetic Lethality in Cancer.bioRxiv : the preprint server for biology · 2025Article
- APOBEC3A drives deaminase mutagenesis in human gastric epithelium.Genome research · 2025Article
- Sensitive, direct detection of non-coding off-target base editor unwinding and editing in primary cells.bioRxiv : the preprint server for biology · 2025Article
- Tobacco smoke carcinogens exacerbate APOBEC mutagenesis and carcinogenesis.Research square · 2025Article
- APOBEC affects tumor evolution and age at onset of lung cancer in smokers.Nature communications · 2025Article
- Evaluating topography of mutational signatures with SigProfilerTopography.Genome biology · 2025Article
- Mechanism of DNA replication fork breakage and PARP1 hyperactivation during replication catastrophe.Science advances · 2025Article
- Article
- APOBEC3B Does Not Promote Tumor Progression in Tp53 Hemizygous Mice.Cancer reports (Hoboken, N.J.) · 2025Article
- Next generation APOBEC3 inhibitors: optimally designed for potency and nuclease stability.Nucleic acids research · 2025Article
- Tobacco smoke carcinogens exacerbate APOBEC mutagenesis and carcinogenesis.bioRxiv : the preprint server for biology · 2025Article
96 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
6 authors at 2 institutions in 1 country.
Funding
Abstract
APOBEC family cytidine deaminases have recently been implicated as powerful mutators of cancer genomes. How APOBECs, which are ssDNA-specific enzymes, gain access to chromosomal DNA is unclear. To ascertain the chromosomal ssDNA substrates of the APOBECs, we expressed APOBEC3A and APOBEC3B, the two most probable APOBECs mediating cancer mutagenesis, in a yeast model system. We demonstrate, using mutation reporters and whole genome sequencing, that APOBEC3A- and APOBEC3B-induced mutagenesis primarily results from the deamination of the lagging strand template during DNA replication. Moreover, our results indicate that both genetic deficiencies in replication fork-stabilizing proteins and chemical induction of replication stress greatly augment the mutagenesis of APOBEC3A and APOBEC3B. Taken together, these results strongly indicate that ssDNA formed during DNA lagging strand synthesis is a major substrate for APOBECs and may be the principal substrate in human cancers experiencing replication stress.
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.