Evidence map›Paper›PMID 42120494›Full record

ArticleEMBO molecular medicine2026

CCDC174 deficiency impaired human fertility by affecting the alternative splicing of maternal mRNAs.

Weijie Wang, Zhiqi Pan, Huixia Jing, Rong Shi, Ling Wu, Jinjie Wang, Biaobang Chen, Jian Mu, Zhihua Zhang, Tianyu Wu and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EMBO molecular medicine, 2026. 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

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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

16 authors.

Weijie Wang *International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. wangweijie0816@126.com.ORCID 0000-0002-5717-1818
Zhiqi Pan *Institute of Pediatrics, Children's Hospital of Fudan University, The Institutes of Biomedical Sciences, State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China.
Huixia Jing *Institute of Pediatrics, Children's Hospital of Fudan University, The Institutes of Biomedical Sciences, State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China.
Rong Shi *Reproductive Medicine Center, Shaanxi Maternal and Child Care Service Center, Xi'an, China.
Ling Wu *Department of Assisted Reproduction, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jinjie WangInstitute of Pediatrics, Children's Hospital of Fudan University, The Institutes of Biomedical Sciences, State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China.
Biaobang ChenInstitute of Pediatrics, Children's Hospital of Fudan University, The Institutes of Biomedical Sciences, State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China.ORCID 0000-0002-9921-2155
Jian MuInstitute of Pediatrics, Children's Hospital of Fudan University, The Institutes of Biomedical Sciences, State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China.
Zhihua ZhangInstitute of Pediatrics, Children's Hospital of Fudan University, The Institutes of Biomedical Sciences, State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China.
Tianyu WuInstitute of Pediatrics, Children's Hospital of Fudan University, The Institutes of Biomedical Sciences, State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China.ORCID 0000-0002-4295-7172
Qiaoli LiInstitute of Pediatrics, Children's Hospital of Fudan University, The Institutes of Biomedical Sciences, State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China.
Juanzi ShiReproductive Medicine Center, Shaanxi Maternal and Child Care Service Center, Xi'an, China.
Yanping KuangDepartment of Assisted Reproduction, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Lin HeBio-X Center, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, China.
Lei WangInstitute of Pediatrics, Children's Hospital of Fudan University, The Institutes of Biomedical Sciences, State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China. wangleiwanglei@fudan.edu.cn.ORCID 0000-0002-3400-0434
Qing SangInstitute of Pediatrics, Children's Hospital of Fudan University, The Institutes of Biomedical Sciences, State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China. sangqing@fudan.edu.cn.ORCID 0000-0002-9895-1394

Funding

Fundamental and Interdisciplinary Disciplines Breakthrough Plan of the Ministry of Education of China No. JYB2025XDXM508Fund of Fudan University and Cao'ejiang Basic Research 24FCB01MOST | National Key Research and Development Program of China (NKPs) 2024YFC2706600MOST | National Natural Science Foundation of China (NSFC) 32130029MOST | National Natural Science Foundation of China (NSFC) 82288102MOST | National Natural Science Foundation of China (NSFC) 82325021MOST | National Natural Science Foundation of China (NSFC) 82422033MOST | National Natural Science Foundation of China (NSFC) 82471885
6 · The paper itself

Abstract

Precise regulation of alternative splicing (AS) of maternal mRNAs is crucial for maintaining mRNA homeostasis and for acquiring oocyte competence. However, the regulatory factors and mechanisms of AS regulating oocyte competence and human fertility remain largely unknown. Here, we identified biallelic variants in CCDC174 that cause human oocyte competence defects and female infertility. Oocyte-specific knockout of Ccdc174 resulted in oocyte maturation arrest and female infertility in mice, and transcriptomic and proteomic analyses indicated that deletion of Ccdc174 disrupted mRNA and protein homeostasis as well as AS in oocytes. Importantly, we found that CCDC174 interacted with the splicing machinery-related PRP19/CDC5L complex, and loss of CCDC174 led to aberrant activation of the expression of these complex members in oocytes. In addition, in vitro studies indicated that patient-derived variants impaired the expression of CCDC174 and its binding to RNAs or CDC5L. Taken together, our study not only show that CCDC174 is a novel AS regulator that maintains mRNA homeostasis and oocyte competence, but also decipher the critical role of CCDC174 deficiency in the pathogenesis of female infertility.

Indexed as

Alternative SplicingFertilityInfertility, FemaleOocytesRNA, MessengerAnimalsFemaleHumansMiceMice, KnockoutRNA, Messenger

Identifiers

PMID42120494
PMCPMC13270137

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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.