ArticleNAR cancer2020
Single-nucleotide polymorphism of the DNA cytosine deaminase APOBEC3H haplotype I leads to enzyme destabilization and correlates with lung cancer.
Article in NAR cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Guardian ubiquitin E3 ligases target cancer-associated APOBEC3 deaminases for degradation to promote human genome integrity.Nature communications · 2026Article
- Machine learning-driven classification and prognostic prediction of kidney renal clear cell carcinoma using APOBEC family expression signatures.Scientific reports · 2025Article
- Comparison of Magnesium and Manganese Ions on the Structural and Catalytic Properties of Human DNA Polymerase Gamma.Journal of chemical theory and computation · 2025Article
- When theory came first: a review of theoretical chemical predictions ahead of experiments.Pure and applied chemistry. Chimie pure et appliquee · 2025Review
- Computational studies on the functional and structural impact of pathogenic mutations in enzymes.Protein science : a publication of the Protein Society · 2025Review
- Differential effects on tumor progression by APOBEC3A, APOBEC3B, and APOBEC3H Haplotype I in a breast cancer mouse xenograft model.Frontiers in genetics · 2025Article
- Mutational impact of APOBEC3A and APOBEC3B in a human cell line and comparisons to breast cancer.PLoS genetics · 2023Article
- APOBEC3-mediated mutagenesis in cancer: causes, clinical significance and therapeutic potential.Journal of hematology & oncology · 2023Review
- Similar deamination activities but different phenotypic outcomes induced by APOBEC3 enzymes in breast epithelial cells.Frontiers in genome editing · 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
- Computational compensatory mutation discovery approach: Predicting a PARP1 variant rescue mutation.Biophysical journal · 2022Article
- Review
- The construction and validation of an RNA binding protein-related prognostic model for bladder cancer.BMC cancer · 2021Article
- APOBEC1 cytosine deaminase activity on single-stranded DNA is suppressed by replication protein A.Nucleic acids research · 2021Article
- The interesting relationship between APOBEC3 deoxycytidine deaminases and cancer: a long road ahead.Open biology · 2020Article
- Computational Investigation of APOBEC3H Substrate Orientation and Selectivity.The journal of physical chemistry. B · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
A number of APOBEC family DNA cytosine deaminases can induce mutations in tumor cells. APOBEC3H haplotype I is one of the deaminases that has been proposed to cause mutations in lung cancer. Here, we confirmed that APOBEC3H haplotype I can cause uracil-induced DNA damage in lung cancer cells that results in γH2AX foci. Interestingly, the database of cancer biomarkers in DNA repair genes (DNArCdb) identified a single-nucleotide polymorphism (rs139298) of APOBEC3H haplotype I that is involved in lung cancer. While we thought this may increase the activity of APOBEC3H haplotype I, instead we found through computational modeling and cell-based experiments that this single-nucleotide polymorphism causes the destabilization of APOBEC3H Haplotype I. Computational analysis suggests that the resulting K121E change affects the structure of APOBEC3H leading to active site disruption and destabilization of the RNA-mediated dimer interface. A K117E mutation in a K121E background stabilized the APOBEC3H haplotype I, thus enabling biochemical study. Subsequent analysis showed that K121E affected catalytic activity, single-stranded DNA binding and oligomerization on single-stranded DNA. The destabilization of a DNA mutator associated with lung cancer supports the model that too much APOBEC3-induced mutation could result in immune recognition or death of tumor cells.
Identifiers
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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.