Evidence map›Paper›PMID 39769018›Full record

ArticleInternational journal of molecular sciences2024

DEAD/H Box 5 (DDX5) Augments E2F1-Induced Cell Death Independent of the Tumor Suppressor p53.

Rinka Nakajima, Yaxuan Zhou, Mashiro Shirasawa, Naoyasu Nishimura, Lin Zhao, Mariana Fikriyanti, Yuki Kamiya, Ritsuko Iwanaga, Andrew P Bradford, Kaori Shinmyozu and 5 more

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. 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

15 authors.

Rinka NakajimaDepartment of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Hyogo, 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, Hyogo, 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, Hyogo, Japan.
Naoyasu NishimuraDepartment of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Hyogo, Japan.
Lin ZhaoDepartment of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Hyogo, Japan.
Mariana FikriyantiDepartment of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Hyogo, Japan.
Yuki KamiyaDepartment of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Hyogo, 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
Kaori ShinmyozuProteomics Support Unit, RIKEN Center for Developmental Biology, Kobe 650-0047, Hyogo, Japan.
Gohei NishibuchiLaboratory of Stem Cell Genetics, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Kyoto, Japan.ORCID 0000-0002-8892-1386
Jun-Ichi NakayamaDivision of Chromatin Regulation, National Institute for Basic Biology, Okazaki 444-8585, Aichi, Japan.ORCID 0000-0002-5597-8239
Kenta KurayoshiDivision of Molecular Genetics, Cancer Research Institute, Kanazawa University, Kakuma-machi, Kanazawa 920-1192, Ishikawa, Japan.
Keigo ArakiDepartment of Morphological Biology, Ohu University School of Dentistry, 31-1 Misumido Tomitamachi, Koriyama 963-8611, Fukushima, Japan.
Kiyoshi OhtaniDepartment of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Hyogo, Japan.

Funding

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

Abstract

In almost all cancers, the p53 pathway is disabled and cancer cells survive. Hence, it is crucially important to induce cell death independent of p53 in the treatment of cancers. The transcription factor E2F1 is controlled by binding of the tumor suppressor pRB, and induces apoptosis by activating the

Indexed as

DEAD-box RNA HelicasesE2F1 Transcription FactorTumor Suppressor Protein p53ApoptosisCell DeathCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansDdx5 protein, humanDEAD-box RNA HelicasesE2F1 protein, humanE2F1 Transcription FactorTP53 protein, humanTumor Suppressor Protein p53ARFBIMcell deathDDX5E2F1p53pRBTAp73

Identifiers

PMID39769018
PMCPMC11675670

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.