Evidence map›Paper›PMID 25875095›Full record

ArticlePloS one2015

A novel transcriptional factor Nkapl is a germ cell-specific suppressor of Notch signaling and is indispensable for spermatogenesis.

Hidenobu Okuda, Hiroshi Kiuchi, Tetsuya Takao, Yasushi Miyagawa, Akira Tsujimura, Norio Nonomura, Haruhiko Miyata, Masaru Okabe, Masahito Ikawa, Yoshitaka Kawakami and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.2field-weighted citation impact, top 7% of its field
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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Science advances · 2025
    Article
  6. Article
  7. Article
  8. The Relationship between The Expression of SpermInternational journal of fertility & sterility · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
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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

13 authors at 4 institutions in 1 country.

Hidenobu OkudaDepartment of Urology, Osaka University Graduate School of Medicine, Osaka, Japan.
Hiroshi KiuchiDepartment of Urology, Osaka University Graduate School of Medicine, Osaka, Japan.
Tetsuya TakaoDepartment of Urology, Osaka University Graduate School of Medicine, Osaka, Japan.
Yasushi MiyagawaDepartment of Urology, Osaka University Graduate School of Medicine, Osaka, Japan.
Akira TsujimuraDepartment of Urology, Juntendo University Hospital, Tokyo, Japan.
Norio NonomuraDepartment of Urology, Osaka University Graduate School of Medicine, Osaka, Japan.
Haruhiko MiyataAnimal Resource Center for Infectious Diseases, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Masaru OkabeAnimal Resource Center for Infectious Diseases, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Masahito IkawaAnimal Resource Center for Infectious Diseases, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Yoshitaka KawakamiNational Institute of Advanced Industrial Science and Technology, Tokyo, Japan.
Naoki GoshimaNational Institute of Advanced Industrial Science and Technology, Tokyo, Japan.
Morimasa WadaMolecular Biology Division, Faculty of Pharmaceutical Sciences, Nagasaki International University, Nagasaki, Japan.
Hiromitsu TanakaMolecular Biology Division, Faculty of Pharmaceutical Sciences, Nagasaki International University, Nagasaki, Japan.
Osaka University · JPNagasaki International University · JPNational Institute of Advanced Industrial Science and Technology · JPJuntendo University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spermatogenesis is an elaborately regulated system dedicated to the continuous production of spermatozoa via the genesis of spermatogonia. In this process, a variety of genes are expressed that are relevant to the differentiation of germ cells at each stage. Although Notch signaling plays a critical role in germ cell development in Drosophila and Caenorhabditis elegans, its function and importance for spermatogenesis in mammals is controversial. We report that Nkapl is a novel germ cell-specific transcriptional suppressor in Notch signaling. It is also associated with several molecules of the Notch corepressor complex such as CIR, HDAC3, and CSL. It was expressed robustly in spermatogonia and early spermatocytes after the age of 3 weeks. Nkapl-deleted mice showed complete arrest at the level of pachytene spermatocytes. In addition, apoptosis was observed in this cell type. Overexpression of NKAPL in germline stem cells demonstrated that Nkapl induced changes in spermatogonial stem cell (SSC) markers and the reduction of differentiation factors through the Notch signaling pathway, whereas testes with Nkapl deleted showed inverse changes in those markers and factors. Therefore, Nkapl is indispensable because aberrantly elevated Notch signaling has negative effects on spermatogenesis, affecting SSC maintenance and differentiation factors. Notch signaling should be properly regulated through the transcriptional factor Nkapl.

Indexed as

AnimalsApoptosisBasic Helix-Loop-Helix ProteinsCell DifferentiationCell LineCell NucleusCo-Repressor ProteinsGerm CellsHEK293 CellsHomeodomain ProteinsHumansMaleMiceMice, Inbred ICRNuclear ProteinsPhenotypeBasic Helix-Loop-Helix ProteinsCo-Repressor ProteinsHes1 protein, mouseHes5 protein, mouseHomeodomain ProteinsNKAPL protein, humanNuclear ProteinsReceptors, NotchRepressor ProteinsRNA, MessengerTranscription Factor HES-1

Identifiers

PMID25875095
PMCPMC4397068
OpenAlexW1973662630

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LicenceCC BY
Read underepoch 390

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.