ArticleNucleic acids research2026
RECQ4 arginine methylation suppresses single-stranded DNA gap accumulation at replication forks.
Article in Nucleic acids research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
The role of protein arginine methylation in regulating transcription and RNA processing is well established, but its function in DNA replication remains poorly understood. In this study, we identify asymmetric dimethylarginine (aDMA) modification of the RECQ4 helicase as a key mechanism linking arginine methylation to replication control. Five arginine residues located within a glycine/arginine-rich region adjacent to the helicase domain of RECQ4 are targeted by type I PRMTs. This modification is enriched during S phase and promotes nuclear localization of RECQ4. On chromatin, aDMA modification is not required for replication origin firing but instead stabilizes the association of DNA polymerase δ with the MCM2-7 replicative helicase complex, thereby ensuring faithful replication fork progression. Mutation of the aDMA-modified residues (the 5RK mutant) leads to aberrant replication complexes and accumulation of single-stranded DNA gaps, resulting in slowed replication fork progression. These defects trigger G2/M arrest and increased anaphase bridge formation, consistent with incomplete DNA replication. Furthermore, cells expressing the 5RK mutant exhibit reduced sensitivity to the PRMT inhibitor MS023, highlighting disruption of RECQ4 methylation-mediated genome stability as a key mechanism underlying MS023-induced cytotoxicity.
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.