Evidence map›Paper›PMID 39117746›Full record

ArticleScientific reports2024

Involvement of the splicing factor SART1 in the BRCA1-dependent homologous recombination repair of DNA double-strand breaks.

Kie Ozaki, Reona Kato, Takaaki Yasuhara, Yuki Uchihara, Miyako Hirakawa, Yu Abe, Hiroki Shibata, Reika Kawabata-Iwakawa, Aizhan Shakayeva, Palina Kot and 5 more

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In one paragraph

Article in Scientific reports, 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.

Kie OzakiHospital Campus Laboratory, Radioisotope Center, Central Institute of Radioisotope Science and Safety Management, Kyushu University, Fukuoka, 812-8582, Japan.
Reona KatoLaboratory of Molecular Radiology, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Takaaki YasuharaLaboratory of Genome Stress Response, Department of Late Effects Studies, Radiation Biology Center, Graduate School of Biostudies, Kyoto University, Sakyo-Ku, Kyoto, 606-8501, Japan.
Yuki UchiharaSignal Transduction Program, Gunma University Initiative for Advanced Research (GIAR), Gunma University, Maebashi, Gunma, 371-8511, Japan.
Miyako HirakawaCenter for Radiation Research and Education, Nagasaki University, Nagasaki, 852-8523, Japan.
Yu AbeDepartment of Radiation Biology and Protection, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, 852-8523, Japan.
Hiroki ShibataDivision of Genomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, 812-8582, Japan.
Reika Kawabata-IwakawaDivision of Integrated Oncology Research, Gunma University Initiative for Advanced Research (GIAR), Gunma University, Maebashi, Gunma, 371-8511, Japan.
Aizhan ShakayevaGraduate School of Biomedical Sciences, Nagasaki University, Nagasaki, 852-8523, Japan.
Palina KotGraduate School of Biomedical Sciences, Nagasaki University, Nagasaki, 852-8523, Japan.
Kiyoshi MiyagawaLaboratory of Molecular Radiology, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Keiji SuzukiDepartment of Radiation Medical Sciences, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, 852-8523, Japan.
Naoki MatsudaCenter for Radiation Research and Education, Nagasaki University, Nagasaki, 852-8523, Japan.
Atsushi ShibataSignal Transduction Program, Gunma University Initiative for Advanced Research (GIAR), Gunma University, Maebashi, Gunma, 371-8511, Japan.
Motohiro YamauchiHospital Campus Laboratory, Radioisotope Center, Central Institute of Radioisotope Science and Safety Management, Kyushu University, Fukuoka, 812-8582, Japan. yamauchi.motohiro.619@m.kyushu-u.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although previous studies have reported that pre-mRNA splicing factors (SFs) are involved in the repair of DNA double-strand breaks (DSBs) via homologous recombination (HR), their exact role in promoting HR remains poorly understood. Here, we showed that SART1, an SF upregulated in several types of cancer, promotes DSB end resection, an essential first step of HR. The resection-promoting function of SART1 requires phosphorylation at threonine 430 and 695 by ATM/ATR. SART1 is recruited to DSB sites in a manner dependent on transcription and its RS domain. SART1 is epistatic with BRCA1, a major HR factor, in the promotion of resection, especially transcription-associated resection in the G2 phase. SART1 and BRCA1 accumulate at DSB sites in an interdependent manner, and epistatically counteract the resection blockade posed by 53BP1 and RIF1. Furthermore, chromosome analysis demonstrated that SART1 and BRCA1 epistatically suppressed genomic alterations caused by DSB misrepair in the G2 phase. Collectively, these results indicate that SART1 and BRCA1 cooperatively facilitate resection of DSBs arising in transcriptionally active genomic regions in the G2 phase, thereby promoting faithful repair by HR, and suppressing genome instability.

Indexed as

BRCA1 ProteinDNA Breaks, Double-StrandedRecombinational DNA RepairAtaxia Telangiectasia Mutated ProteinsCell Line, TumorEpistasis, GeneticG2 PhaseHumansPhosphorylationSerine-Arginine Splicing FactorsTelomere-Binding ProteinsTumor Suppressor p53-Binding Protein 1Ataxia Telangiectasia Mutated ProteinsATM protein, humanATR protein, humanBRCA1 ProteinBRCA1 protein, humanRif1 protein, humanSerine-Arginine Splicing FactorsTelomere-Binding ProteinsTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1

Identifiers

PMID39117746
PMCPMC11310344

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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.