ArticleNucleic acids research2017
Self-cytoplasmic DNA upregulates the mutator enzyme APOBEC3A leading to chromosomal DNA damage.
Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed.
- 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
- Hypoxia-mimicked mitochondrial stress triggers APOBEC3A-mediated DNA damage via non-canonical innate immune activation.NAR molecular medicine · 2026Article
- The Distinct Monocyte Subsets and Intercellular Communication in Primary Sjögren's Syndrome Revealed by Single-Cell RNA Sequencing.Journal of clinical immunology · 2025Article
- 3A or not 3A: Cytidine deaminases in the etiology of the CAG-repeat expansion diseases.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Unraveling the role of lncRNAs and their associated nearby coding genes in the pathogenesis of systemic lupus erythematosus.Arthritis research & therapy · 2025Article
- Article
- An overview of the functions and mechanisms of APOBEC3A in tumorigenesis.Acta pharmaceutica Sinica. B · 2024Review
- Her2 amplification, Rel-A, and Bach1 can influence APOBEC3A expression in breast cancer cells.PLoS genetics · 2024Article
- Critical contribution of mitochondria in the development of cardiomyopathy linked to desmin mutation.Stem cell research & therapy · 2024Article
- Monitoring APOBEC3A protein levels in human cancer cells.Methods in cell biology · 2024Article
- Regulatory factor X1 induces macrophage M1 polarization by promoting DNA demethylation in autoimmune inflammation.JCI insight · 2023Article
- DNA Deamination Is Required for Human APOBEC3A-Driven Hepatocellular Carcinoma In Vivo.International journal of molecular sciences · 2023Article
- Antagonism of ALAS1 by the Measles Virus V protein contributes to degradation of the mitochondrial network and promotes interferon response.PLoS pathogens · 2023Article
- Evolution of the RNA Cleavage Subunit C11/RPC10, and Recycling by RNA Polymerase III.Journal of cellular immunology · 2022Article
- Roles of APOBEC3 in hepatitis B virus (HBV) infection and hepatocarcinogenesis.Bioengineered · 2021Review
- Genotoxic stress and viral infection induce transient expression of APOBEC3A and pro-inflammatory genes through two distinct pathways.Nature communications · 2021Article
- Sustained high expression of multiple APOBEC3 cytidine deaminases in systemic lupus erythematosus.Scientific reports · 2021Article
- Activation of NF-κB signaling via cytosolic mitochondrial RNA sensing in kerotocytes with mitochondrial DNA common deletion.Scientific reports · 2021Article
- An extended APOBEC3A mutation signature in cancer.Nature communications · 2021Article
- Molecular origins of APOBEC-associated mutations in cancer.DNA repair · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Foreign and self-cytoplasmic DNA are recognized by numerous DNA sensor molecules leading to the production of type I interferons. Such DNA agonists should be degraded otherwise cells would be chronically stressed. Most human APOBEC3 cytidine deaminases can initiate catabolism of cytoplasmic mitochondrial DNA. Using the human myeloid cell line THP-1 with an interferon inducible APOBEC3A gene, we show that cytoplasmic DNA triggers interferon α and β production through the RNA polymerase III transcription/RIG-I pathway leading to massive upregulation of APOBEC3A. By catalyzing C→U editing in single stranded DNA fragments, the enzyme prevents them from re-annealing so attenuating the danger signal. The price to pay is chromosomal DNA damage in the form of CG→TA mutations and double stranded DNA breaks which, in the context of chronic inflammation, could drive cells down the path toward cancer.
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.