Evidence map›Paper›PMID 40707437›Full record

ArticleCell death discovery2025

Strawberry notch 1 safeguards neuronal genome via regulation of Yeats4 expression.

Dai Ihara, Ayano Narumoto, Yukie Kande, Tomoki Hayashi, Yasuaki Ikuno, Manabu Shirai, Masaki Wakabayashi, Ryo Nitta, Hayato Naka-Kaneda, Yu Katsuyama

Abstract read
In one paragraph

Article in Cell death discovery, 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

10 authors.

Dai Ihara *Department of Anatomy, Shiga University of Medical Science, Shiga, Japan. daiihara@belle.shiga-med.ac.jp.ORCID http://orcid.org/0000-0001-6320-1617
Ayano Narumoto *Department of Anatomy, Shiga University of Medical Science, Shiga, Japan.
Yukie KandeDepartment of Anatomy, Shiga University of Medical Science, Shiga, Japan.
Tomoki HayashiDepartment of Anatomy, Shiga University of Medical Science, Shiga, Japan.
Yasuaki IkunoDepartment of Anatomy, Shiga University of Medical Science, Shiga, Japan.
Manabu ShiraiOmics Research Center, National Cerebral and Cardiovascular Center, Osaka, Japan.ORCID http://orcid.org/0000-0002-1063-5822
Masaki WakabayashiOmics Research Center, National Cerebral and Cardiovascular Center, Osaka, Japan.
Ryo NittaDivision of Structural Medicine and Anatomy, Department of Physiology and Cell Biology, Kobe University Graduate School of Medicine, Kobe, Japan.
Hayato Naka-KanedaDepartment of Anatomy, Shiga University of Medical Science, Shiga, Japan.ORCID http://orcid.org/0000-0003-3764-6238
Yu KatsuyamaDepartment of Anatomy, Shiga University of Medical Science, Shiga, Japan. kats@belle.shiga-med.ac.jp.

Funding

MEXT | Japan Society for the Promotion of Science (JSPS) 20K22735MEXT | Japan Society for the Promotion of Science (JSPS) 21K15331MEXT | Japan Society for the Promotion of Science (JSPS) 25K18701
6 · The paper itself

Abstract

Neurons are subjected to various stresses, including high metabolic demand, physiological activity, and transcriptional regulation, to which their genomic DNA are vulnerable. Genome stability of neurons is essential for proper physiological brain function. Failure in accurate genomic DNA repair can result in abnormal neuronal functions or cell death. Genomic instability has been implicated in increased risks of neurodevelopmental and neurodegenerative disorders. However, the molecular mechanisms underlying neuronal genome stability remain poorly understood. Mutations in the Strawberry Notch Homolog 1 (SBNO1) have been suggested to contribute to these disorders. Here, we investigated the molecular mechanisms underlying histological abnormalities observed in the cortex of Sbno1 knockout (KO) mice. Comprehensive gene expression analysis revealed that Sbno1 KO affects the expression of genes related to cell survival, consistent with the increased apoptosis observed in Sbno1 KO cortices. Among the genes downregulated in Sbno1 KO, we focused on Yeats4. Overexpression of Yeats4 rescued the accumulation of genomic DNA damage and cell death caused by Sbno1 deletion. These findings suggest that Sbno1 is critical in safeguarding the neuronal genome, at least in part, via regulating Yeats4 expression.

Identifiers

PMID40707437
PMCPMC12289961

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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.