Evidence map›Paper›PMID 39624989›Full record

ArticleGenes to cells : devoted to molecular & cellular mechanisms2025

Defects in the H3t Gene Cause an Increase in Leydig Cells With Impaired Spermatogenesis in Mice.

Qianmei Wu, Miho Ito, Takeru Fujii, Kaori Tanaka, Kohta Nakatani, Yoshihiro Izumi, Takeshi Bamba, Takashi Baba, Kazumitsu Maehara, Kosuke Tomimatsu and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes to cells : devoted to molecular & cellular mechanisms, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Qianmei WuDivision of Transcriptomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Miho ItoDivision of Transcriptomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Takeru FujiiDivision of Transcriptomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Kaori TanakaDivision of Transcriptomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Kohta NakataniDivision of Metabolomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Yoshihiro IzumiDivision of Metabolomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Takeshi BambaDivision of Metabolomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Takashi BabaDepartment of Molecular Biology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Kazumitsu MaeharaDivision of Transcriptomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Kosuke TomimatsuDivision of Transcriptomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Tatsuya TakemotoLaboratory for Embryology, Institute for Advanced Medical Sciences, Tokushima University, Tokushima, Japan.
Yasuyuki OhkawaDivision of Transcriptomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.ORCID https://orcid.org/0000-0001-6440-9954
Akihito HaradaDivision of Transcriptomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.ORCID https://orcid.org/0009-0003-1420-4549

Funding

Advanced Research & Development Programs for Medical Innovation JP23gm1810008Basis for Supporting Innovative Drug Discovery and Life Science Research JP22ama121017j0001Core Research for Evolutional Science and Technology JPMJCR23N3Fusion Oriented Research for Disruptive Science and Technology JPMJFR2251Japan Society for the Promotion of Science JP21H05292Japan Society for the Promotion of Science JP22H03538Japan Society for the Promotion of Science JP22H04676Japan Society for the Promotion of Science JP22H04696Japan Society for the Promotion of Science JP22J20655Japan Society for the Promotion of Science JP22J20675Japan Society for the Promotion of Science JP22K19275Japan Society for the Promotion of Science JP22K19314Japan Society for the Promotion of Science JP23H00372Japan Society for the Promotion of Science JP23H02394Japan Society for the Promotion of Science JP23H04288Japan Society for the Promotion of Science JP23K24795Japan Society for the Promotion of Science JP23K27087Japan Society for the Promotion of Science JP24H02323Medical Research Center Initiative for High Depth OmicsMEXT Interdisciplinary Development Hub Formation Program JPMXP1323015486MEXT Joint Usage/Research Center Pan-Omics DDRICPrecursory Research for Embryonic Science and Technology JPMJPR19K7Precursory Research for Embryonic Science and Technology JPMJPR2026Research Institute for Information Technology, Kyushu University
6 · The paper itself

Abstract

Abnormalities in spermatogenesis, a fundamental component of male reproductive function, can cause male infertility. Somatic cells constituting the testis microenvironment are essential for controlling normal spermatogenesis. Although testicular somatic cells are thought to sense and respond to germ cells to ensure proper spermatogenesis, the details of this signaling mechanism are unknown. Here, we investigated somatic cell dynamics in testicular tissue lacking spermatogenesis using the mice with deletion of the testis-specific histone H3 variant gene H3t. Testicular tissue sections of H3t

Indexed as

HistonesLeydig CellsSpermatogenesisAnimalsInfertility, MaleMaleMiceMice, Inbred C57BLTestisTestosteroneHistonesTestosteroneLeydig cellsspatial transcriptomicsspermatogenesis

Identifiers

PMID39624989
PMCPMC11655955

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.