Evidence map›Paper›PMID 39772743›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2025

APOBEC3A deaminates CTG hairpin loops to promote fragility and instability of expanded CAG/CTG repeats.

Rebecca E Brown, Margo Coxon, Benjamin Larsen, Maxwell Allison, Ariana Chadha, Isabelle Mittelstadt, Tony M Mertz, Steven A Roberts, Catherine H Freudenreich

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Emerging drivers of DNA repeat expansions.Biochemical Society transactions · 2025
    Review
  5. 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 · 2025
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Rebecca E BrownProgram in Genetics, Molecular, and Cellular Biology, Tufts University Graduate School of Biomedical Sciences, Boston, MA 02111.ORCID 0000-0003-0340-8055
Margo Coxon *School of Molecular Biosciences, Washington State University, Pullman, WA 99164.
Benjamin Larsen *Department of Biology, Tufts University, Medford, MA 02155.ORCID 0000-0001-6831-7088
Maxwell AllisonDepartment of Biology, Tufts University, Medford, MA 02155.
Ariana ChadhaDepartment of Biology, Tufts University, Medford, MA 02155.
Isabelle MittelstadtDepartment of Microbiology and Molecular Genetics, Larner College of Medicine, University of Vermont, Burlington, VT 05405.
Tony M MertzSchool of Molecular Biosciences, Washington State University, Pullman, WA 99164.
Steven A RobertsSchool of Molecular Biosciences, Washington State University, Pullman, WA 99164.
Catherine H FreudenreichProgram in Genetics, Molecular, and Cellular Biology, Tufts University Graduate School of Biomedical Sciences, Boston, MA 02111.ORCID 0000-0002-1652-2917

Funding

Mechanisms of genome instability induced by APOBEC Cytidine Deaminases & its impacts during cancer development - Diversity SupplementR01CA218112 · NCI · WASHINGTON STATE UNIVERSITY · PI ROBERTS, STEVEN A · 2017 to 2021
$2.2M
Replication through DNA Structures and Consequences for Genome StabilityR35GM144215 · NIGMS · TUFTS UNIVERSITY MEDFORD · PI CATHERINE H FREUDENREICH · 2022 to 2026
$2.0M
Regulation of APOBEC3 cytidine deaminase-induced mutation during cancerdevelopmentR01CA269784 · NCI · WASHINGTON STATE UNIVERSITY · PI STEVEN A ROBERTS · 2023 to 2026
$2.0M
HHS | NIH | National Cancer Institute (NCI) R01CA218112HHS | NIH | National Cancer Institute (NCI) R01CA269784NCI NIH HHS R01 CA218112NCI NIH HHS R01 CA269784NIGMS NIH HHS R35 GM144215NSF | BIO | Division of Molecular and Cellular Biosciences (MCB) MCB 1817499
6 · The paper itself

Abstract

CAG/CTG repeats are prone to expansion, causing several inherited human diseases. The initiating sources of DNA damage which lead to inaccurate repair of the repeat tract to cause expansions are not fully understood. Expansion-prone CAG/CTG repeats are actively transcribed and prone to forming stable R-loops with hairpin structures forming on the displaced single-stranded DNA (S-loops). We previously determined that damage by the

Indexed as

Cytidine DeaminaseTrinucleotide Repeat ExpansionAICDA (Activation-Induced Cytidine Deaminase)DeaminationDNA DamageGenomic InstabilityHumansMinor Histocompatibility AntigensProteinsR-Loop StructuresSaccharomyces cerevisiaeAICDA (Activation-Induced Cytidine Deaminase)APOBEC3A protein, humanAPOBEC3B protein, humanCytidine DeaminaseMinor Histocompatibility AntigensProteinsAPOBECCAG repeat instabilityHuntington’s diseaseR-looptrinucleotide repeat

Identifiers

PMID39772743
PMCPMC11745325

What OpenQuestion holds

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Registered trials

None linked

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.