Evidence map›Paper›PMID 40869977›Full record

ArticleGenes2025

The Transcriptional Coactivator

Rinka Nakajima, Yaxuan Zhou, Mashiro Shirasawa, Mariana Fikriyanti, Ritsuko Iwanaga, Andrew P Bradford, Kenta Kurayoshi, Keigo Araki, Kiyoshi Ohtani

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Rinka NakajimaDepartment of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Japan.ORCID 0009-0000-3222-7590
Yaxuan ZhouDepartment of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Japan.ORCID 0009-0009-2593-3572
Mashiro ShirasawaDepartment of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Japan.
Mariana FikriyantiDepartment of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Japan.
Ritsuko IwanagaDepartment of Obstetrics and Gynecology, University of Colorado School of Medicine-Anschutz Medical Campus, 12700 East 19th Avenue, Aurora, CO 80045, USA.ORCID 0009-0008-1142-4753
Andrew P BradfordDepartment of Obstetrics and Gynecology, University of Colorado School of Medicine-Anschutz Medical Campus, 12700 East 19th Avenue, Aurora, CO 80045, USA.ORCID 0000-0002-8728-571X
Kenta KurayoshiDivision of Molecular Genetics, Cancer Research Institute, Kanazawa University, Kakuma-Machi, Kanazawa 920-1192, Japan.
Keigo ArakiDepartment of Morphological Biology, Ohu University School of Dentistry, 31-1 Misumido Tomitamachi, Koriyama 963-8611, Japan.
Kiyoshi OhtaniDepartment of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Japan.

Funding

Ministry of Education, Culture, Sports, Science and Technology in Japan 21K07136
6 · The paper itself

Abstract

backgroundDEAD/H box 5 (DDX5) serves as a transcriptional coactivator for several transcription factors including E2F1, the primary target of the tumor suppressor pRB. E2F1 physiologically activated by growth stimulation activates growth-related genes and promotes cell proliferation. In contrast, upon loss of pRB function due to oncogenic changes, E2F1 is activated out of restraint by pRB (deregulated E2F1) and stimulates tumor suppressor genes such as

objectiveWe thus examined whether the

methodFor this purpose, we performed promoter analysis and ChIP assay.

resultThe DDX5 promoter did not possess typical E2F binding consensus but contained several GC repeats observed in deregulated E2F1 targets. Insertion of point mutations in these GC repeats decreased responsiveness to deregulated E2F1 induced by over-expression of E2F1, but scarcely affected responsiveness to growth stimulation. ChIP assays showed that deregulated E2F1 induced by over-expression of E2F1 or expression of E1a, which binds pRB and releases E2F1, bound to the

conclusionsThese results suggest that the

Indexed as

DEAD-box RNA HelicasesE2F1 Transcription FactorRetinoblastoma ProteinCell Line, TumorGene Expression Regulation, NeoplasticHumansPromoter Regions, GeneticDdx5 protein, humanDEAD-box RNA HelicasesE2F1 protein, humanE2F1 Transcription FactorRetinoblastoma ProteinDDX5E2F1gene expressionpRBpromoter analysis

Identifiers

PMID40869977
PMCPMC12385852

What OpenQuestion holds

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Read underepoch 390

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.