ArticleBiochemistry and biophysics reports2018
Onset of deaminase APOBEC3B induction in response to DNA double-strand breaks.
Article in Biochemistry and biophysics reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- APOBEC3B enhances the efficacy of PARP inhibitors in elimination of ovarian cancer stem cell.Scientific reports · 2026Article
- Identification of natural product 3, 5-diiodotyrosine as APOBEC3B inhibitor to prevent somatic mutation accumulation and cancer progression.Journal for immunotherapy of cancer · 2022Article
- KMT2C-deficient tumors have elevated APOBEC mutagenesis and genomic instability in multiple cancers.NAR cancer · 2022Article
- Genes Possessing the Most Frequent DNA DSBs Are Highly Associated with Development and Cancers, and Essentially Overlap with the rDNA-Contacting Genes.International journal of molecular sciences · 2022Article
- Involvement of APOBEC3B in mutation induction by irradiation.Journal of radiation research · 2020Article
- Article
- Network-based approaches elucidate differences within APOBEC and clock-like signatures in breast cancer.Genome medicine · 2020Article
- APOBEC3B reporter myeloma cell lines identify DNA damage response pathways leading to APOBEC3B expression.PloS one · 2020Article
- Hidden Markov models lead to higher resolution maps of mutation signature activity in cancer.Genome medicine · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deamination of 5-methyl cytosine is a major cause of cancer-driver mutations in inflammation-associated cancers. The deaminase APOBEC3B is expressed in these cancers and causes mutations under replication stress; however, the mechanisms by which APOBEC3B mediates deamination and its association with genomic disorders are still unclear. Here, we show that APOBEC3B is stabilized to induce deamination reaction in response to DNA double-strand breaks (DSBs), resulting in the formation of long-lasting DSBs. Uracil, the major deamination product, is subsequently targeted by base excision repair (BER) through uracil-DNA glycosylase 2 (UNG2); hence late-onset DSBs arise as by-products of BER. The frequency of these delayed DSBs was increased by treatment of cells with a PARP inhibitor, and was suppressed following knock-down of UNG2. The late-onset DSBs were induced in an ATR-dependent manner. Those secondary DSBs were persistent, unlike DSBs directly caused by γ-ray irradiation. Overall, these results suggest that the deaminase APOBEC3B is induced in response to DSBs, leading to long-lasting DSB formation in addition to mutagenic 5me-C>T transition induction.
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