Evidence map›Paper›PMID 40735501›Full record

ArticlemicroPublication biology2025

Regulation of DNA repair gene expression by PRMT5.

Hunter Bliss, Renee A Bouley, Ruben C Petreaca

Abstract read
In one paragraph

Article in microPublication biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Hunter BlissBiology, The Ohio State University.
Renee A BouleyThe Ohio State University.
Ruben C PetreacaThe Ohio State University.

Funding

The role of PRMT5 in preventing intra-chromosomal deletions in cancer cellsR03CA276967 · NCI · OHIO STATE UNIVERSITY · PI BOULEY, RENEE, PETREACA, RUBEN CIPRIAN · 2023 to 2024
$158k
NCI NIH HHS R03 CA276967
6 · The paper itself

Abstract

PRMT5 is a member of a class of enzymes called protein arginine methyltransferases (PRMTs) that play a role in maintaining genomic stability through post-translational modification of components of the TIP60 chromatin remodeling super complex. TIP60 is required primarily for chromatin remodeling at DNA double-strand breaks. Mutations in either TIP60 or PRMT5 affect repair by homologous recombination. A recent study has shown that in leukemia and lymphoma, PRMT5 also controls mRNA expression of TIP60 and other DNA repair genes by regulating alternative splicing. This analysis utilizes publicly available data from the Catalogue of Somatic Mutations in Cancer (COSMIC) to interrogate how PRMT5 expression correlates with expression levels of other key DNA repair genes: KAT5 (TIP60), H2A (H2AFX), TP53, TP53BP1, and RAD51 in all cancers. We find that indeed an increase in PRMT5 expression levels correlates with an increase in KAT5 levels. A weak correlation was also observed between PRMT5 and TP53, TP53BP1, and RAD51. These findings extend previous PRMT5 roles in controlling gene expression to all cancer types and further highlight the role of this enzyme not only in post-translational modification but also regulation of gene expression.

Identifiers

PMID40735501
PMCPMC12305363

What OpenQuestion holds

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Registered trials

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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.