Evidence map›Paper›PMID 40095067›Full record

ArticleCellular and molecular life sciences : CMLS2025

Loss of Cep135 causes oligoasthenoteratozoospermia and male infertility in mice.

Hui Liu, Haozheng Zhang, Guanghao Qin, Tingting Song, Xin Liu, Zongzhuang Wen, Min Liu, Xianmei Wang, Xiaolong Fu, Jiangang Gao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

10 authors.

Hui LiuDepartment of Histology and Embryology, School of Clinical and Basic Medical Sciences, Shandong First Medical University & Shandong Academy of Medical Science, Jinan, Shandong, China.
Haozheng ZhangChildren's Hospital Affiliated to Shandong University, Jinan, Shandong, China.
Guanghao QinDepartment of Histology and Embryology, School of Clinical and Basic Medical Sciences, Shandong First Medical University & Shandong Academy of Medical Science, Jinan, Shandong, China.
Tingting SongDepartment of Histology and Embryology, School of Clinical and Basic Medical Sciences, Shandong First Medical University & Shandong Academy of Medical Science, Jinan, Shandong, China.
Xin LiuDepartment of Histology and Embryology, School of Clinical and Basic Medical Sciences, Shandong First Medical University & Shandong Academy of Medical Science, Jinan, Shandong, China.
Zongzhuang WenCentral Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Min LiuThe Affiliated Taian City Central Hospital of Qingdao University, Taian, China. Justdoit.66@163.com.
Xianmei WangCentral Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China. wangxianmei0123@126.com.
Xiaolong FuDepartment of Histology and Embryology, School of Clinical and Basic Medical Sciences, Shandong First Medical University & Shandong Academy of Medical Science, Jinan, Shandong, China. fuxiaolong@sdfmu.edu.cn.
Jiangang GaoCentral Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China. jggao@sdu.edu.cn.ORCID http://orcid.org/0000-0001-6619-7107

Funding

National Natural Science Foundation of China 82401875Natural Science Foundation of Shandong Province ZR2022QC184Natural Science Foundation of Shandong Province ZR2023QH164Science and Technology Support Plan for Youth Innovation of Colleges and Universities of Shandong Province of China 202201010631Science and Technology Support Plan for Youth Innovation of Colleges and Universities of Shandong Province of China 202205030999Shandong First Medical University 202201-010
6 · The paper itself

Abstract

Centrosomal proteins (Cep), as crucial scaffolding molecules, play a pivotal role in the biogenesis of centrioles and the regulation of the cell cycle. To date, mutation in Cep135 has been reported to be closely associated with multiple morphological abnormalities of the flagella (MMAF) in humans. However, the specific mechanism of Cep135 in spermatogenesis and its detailed role in male infertility remains largely unexplored. In this study, we present compelling evidence that Cep135 functions as a pathogenic gene responsible for oligoasthenoteratozoospermia (OAT) and male infertility in mice. By selectively deleting Cep135 in premeiotic germ cells using Stra8-Cre mice crossed with Cep135

Indexed as

AsthenozoospermiaCell Cycle ProteinsInfertility, MaleOligospermiaAcrosomeA Kinase Anchor ProteinsAnimalsApoptosisMaleMiceMice, Inbred C57BLMice, KnockoutMicrotubule ProteinsSpermatogenesisSpermatozoaSperm TailA Kinase Anchor ProteinsCell Cycle ProteinsMicrotubule ProteinsSPAG6 protein, mouseMale infertilityMouse modelOligoasthenoteratozoospermiaSpermSpermatogenesis

Identifiers

PMID40095067
PMCPMC11914644

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.