ArticleBlood2012
APOBEC3G enhances lymphoma cell radioresistance by promoting cytidine deaminase-dependent DNA repair.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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The trial behind it
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Who cites it
47 citing papers in PubMed, 66 citations in OpenAlex.
- Differential effects on tumor progression by APOBEC3A, APOBEC3B, and APOBEC3H Haplotype I in a breast cancer mouse xenograft model.Frontiers in genetics · 2025Article
- Cytidine deaminases APOBEC3C and APOBEC3D promote DNA replication stress resistance in pancreatic cancer cells.Nature cancer · 2024Article
- APOBEC3G protects the genome of human cultured cells and mice from radiation-induced damage.The FEBS journal · 2023Article
- Similar deamination activities but different phenotypic outcomes induced by APOBEC3 enzymes in breast epithelial cells.Frontiers in genome editing · 2023Article
- Screening of Lymphoma Radiotherapy-Resistant Genes with CRISPR Activation Library.Pharmacogenomics and personalized medicine · 2023Article
- Competition for DNA binding between the genome protector replication protein A and the genome modifying APOBEC3 single-stranded DNA deaminases.Nucleic acids research · 2022Article
- Aberrant APOBEC3C expression induces characteristic genomic instability in pancreatic ductal adenocarcinoma.Oncogenesis · 2022Article
- Radiosensitization to γ-Ray by Functional Inhibition of APOBEC3G.International journal of molecular sciences · 2022Article
- APOBEC3C, a nucleolar protein induced by genotoxins, is excluded from DNA damage sites.The FEBS journal · 2022Article
- Mutagenic Activity of AID/APOBEC Deaminases in Antiviral Defense and Carcinogenesis.Molecular biology · 2022Article
- Roles of APOBEC3 in hepatitis B virus (HBV) infection and hepatocarcinogenesis.Bioengineered · 2021Review
- Dysregulated APOBEC3G causes DNA damage and promotes genomic instability in multiple myeloma.Blood cancer journal · 2021Article
- Radiotherapy is associated with a deletion signature that contributes to poor outcomes in patients with cancer.Nature genetics · 2021Article
- FDG PET/CT parameters and correlations with tumor-absorbed doses in a phase 1 trial ofEuropean journal of nuclear medicine and molecular imaging · 2021Article
- Induction of APOBEC3B expression by chemotherapy drugs is mediated by DNA-PK-directed activation of NF-κB.Oncogene · 2021Article
- miRNA signature associated with R-CHOP refractoriness in patients diagnosed with diffuse large B cell lymphoma.Non-coding RNA research · 2020Article
- The interesting relationship between APOBEC3 deoxycytidine deaminases and cancer: a long road ahead.Open biology · 2020Article
- APOBEC3 enzymes mediate efficacy of cisplatin and are epistatic with base excision repair and mismatch repair in platinum response.NAR cancer · 2020Article
- Involvement of APOBEC3B in mutation induction by irradiation.Journal of radiation research · 2020Article
- Changes in the Radiation Toxicity of Human Lymphoblastic T-cell Line (Jurkat) by a Common Pesticide: Diazinon.Journal of biomedical physics & engineering · 2020Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
APOBEC3 proteins catalyze deamination of cytidines in single-stranded DNA (ssDNA), providing innate protection against retroviral replication by inducing deleterious dC > dU hypermutation of replication intermediates. APOBEC3G expression is induced in mitogen-activated lymphocytes; however, no physiologic role related to lymphoid cell proliferation has yet to be determined. Moreover, whether APOBEC3G cytidine deaminase activity transcends to processing cellular genomic DNA is unknown. Here we show that lymphoma cells expressing high APOBEC3G levels display efficient repair of genomic DNA double-strand breaks (DSBs) induced by ionizing radiation and enhanced survival of irradiated cells. APOBEC3G transiently accumulated in the nucleus in response to ionizing radiation and was recruited to DSB repair foci. Consistent with a direct role in DSB repair, inhibition of APOBEC3G expression or deaminase activity resulted in deficient DSB repair, whereas reconstitution of APOBEC3G expression in leukemia cells enhanced DSB repair. APOBEC3G activity involved processing of DNA flanking a DSB in an integrated reporter cassette. Atomic force microscopy indicated that APOBEC3G multimers associate with ssDNA termini, triggering multimer disassembly to multiple catalytic units. These results identify APOBEC3G as a prosurvival factor in lymphoma cells, marking APOBEC3G as a potential target for sensitizing lymphoma to radiation therapy.
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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.