Evidence map›Paper›PMID 39747609›Full record

ArticleScientific reports2025

Heterozygous mutation in BRCA2 induces accelerated age-dependent decline in sperm quality with male subfertility in rats.

Yashiro Motooka, Hideaki Tanaka, Yuki Maeda, Misako Katabuchi, Tomoji Mashimo, Shinya Toyokuni

Abstract read
In one paragraph

Article in Scientific reports, 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. Article
  2. Review
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

6 authors.

Yashiro MotookaDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan. motooka@med.nagoya-u.ac.jp.
Hideaki TanakaDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.
Yuki MaedaDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.
Misako KatabuchiDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.
Tomoji MashimoLaboratory Animal Research Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Shinya ToyokuniDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan. toyokuni@med.nagoya-u.ac.jp.

Funding

Japan Society for the Promotion of Science JP16H06276 [AdAMS (Aa210038)]Japan Society for the Promotion of Science JP19H0546Japan Society for the Promotion of Science JP23K08883JST CREST JPMJCR19H4
6 · The paper itself

Abstract

Tumor suppressor BRCA2 executes homologous recombination to repair DNA double-strand breaks in collaboration with RAD51, involving exon 11 and 27. Exon 11 constitutes a region where pathogenic variants (PVs) accumulate, and mutations in this region are known to contribute to carcinogenesis. However, the impact of the heterozygous PVs of BRCA2 exon 11 on the life quality beyond cancer risk, including male fertility, remains unclear. Here, we established a rat model with a frameshift on the seventh BRC repeat in Brca2 exon 11 (Brca2

Indexed as

BRCA2 ProteinInfertility, MaleSpermatozoaAgingAnimalsApoptosisCRISPR-Cas SystemsDNA Breaks, Double-StrandedExonsHeterozygoteHumansMaleMutationRatsTestisBRCA2 ProteinAgingBRCA2 exon 11HeterozygoteMale subfertilityPathogenic variantSpermatogenesis

Identifiers

PMID39747609
PMCPMC11696240

What OpenQuestion holds

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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.