Evidence map›Paper›PMID 36109592›Full record

ArticleCommunications biology2022

Tmsb10 triggers fetal Leydig differentiation by suppressing the RAS/ERK pathway.

Miki Inoue, Takashi Baba, Fumiya Takahashi, Miho Terao, Shogo Yanai, Yuichi Shima, Daisuke Saito, Kei Sugihara, Takashi Miura, Shuji Takada and 3 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

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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 2 institutions in 1 country.

Miki InoueDepartment of Systems Life Sciences, Graduate School of Systems Life Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.ORCID http://orcid.org/0000-0003-3581-9852
Takashi BabaDepartment of Systems Life Sciences, Graduate School of Systems Life Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Fumiya TakahashiDepartment of Systems Life Sciences, Graduate School of Systems Life Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Miho TeraoDepartment of Systems BioMedicine, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya-ku, Tokyo, 157-8535, Japan.
Shogo YanaiDepartment of Systems Life Sciences, Graduate School of Systems Life Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Yuichi ShimaDepartment of Systems Life Sciences, Graduate School of Systems Life Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Daisuke SaitoDepartment of Systems Life Sciences, Graduate School of Systems Life Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Kei SugiharaDepartment of Anatomy and Cell Biology, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.ORCID http://orcid.org/0000-0002-5502-6967
Takashi MiuraDepartment of Anatomy and Cell Biology, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Shuji TakadaDepartment of Systems BioMedicine, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya-ku, Tokyo, 157-8535, Japan.ORCID http://orcid.org/0000-0002-9406-4683
Mikita SuyamaDepartment of Systems Life Sciences, Graduate School of Systems Life Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.ORCID http://orcid.org/0000-0001-9526-3193
Yasuyuki OhkawaDepartment of Systems Life Sciences, Graduate School of Systems Life Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.ORCID http://orcid.org/0000-0001-6440-9954
Ken-Ichirou MorohashiDepartment of Systems Life Sciences, Graduate School of Systems Life Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan. morohashi.ken-ichirou.874@m.kyushu-u.ac.jp.
Kyushu University · JPNational Center For Child Health and Development · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leydig cells in fetal testes play crucial roles in masculinizing fetuses through androgen production. Gene knockout studies have revealed that growth factors are implicated in fetal Leydig cell (FLC) differentiation, but little is known about the mechanisms regulating this process. We investigate this issue by characterizing FLC progenitor cells using single-cell RNA sequencing. The sequence datasets suggest that thymosin β10 (Tmsb10) is transiently upregulated in the progenitors. While studying the function of Tmsb10, we reveal that platelet-derived growth factor (PDGF) regulates ciliogenesis through the RAS/ERK and PI3K/AKT pathways, and thereby promotes desert hedgehog (DHH)-dependent FLC differentiation. Tmsb10 expressed in the progenitor cells induces their differentiation into FLCs by suppressing the RAS/ERK pathway. Through characterizing the transiently expressed Tmsb10 in the FLC progenitors, this study unveils the molecular process of FLC differentiation and shows that it is cooperatively induced by DHH and PDGF.

Indexed as

AndrogensMAP Kinase Signaling SystemFetusHumansMalePhosphatidylinositol 3-KinasesPlatelet-Derived Growth FactorProto-Oncogene Proteins c-aktras ProteinsThymosinAndrogensPhosphatidylinositol 3-KinasesPlatelet-Derived Growth FactorProto-Oncogene Proteins c-aktras ProteinsThymosinthymosin beta(10)

Identifiers

PMID36109592
PMCPMC9478096
OpenAlexW4296032563

What Socratic holds

Textmetadata
LicenceCC BY
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.