Evidence map›Paper›PMID 40462101›Full record

ArticleJournal of translational medicine2025

Essential roles of DCAF7/WDR68 in mouse embryonic development.

Zhaoxia Wu, Zijun Deng, Shufang Wang, Wanyin Wang

Abstract read
In one paragraph

Article in Journal of translational medicine, 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

4 authors.

Zhaoxia Wu *Digestive Endoscopy Center, Key Laboratory for Translational Research and Innovative Therapeutics of Gastrointestinal Oncology, Hongqiao International Institute of Medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, No. 1111, Xianxia Rd, Changning District, Shanghai, 200336, China. zhaoxiawu@shsmu.edu.cn.ORCID 0000-0002-6224-7477
Zijun Deng *Laboratory of Key Technology and Materials in Minimally Invasive Spine Surgery, Hongqiao International Institute of Medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shufang Wang *Department of Forensic Medicine, Xinxiang Medical University, Xinxiang, Henan Province, China.
Wanyin WangEastern Hepatobiliary Clinical Research Institute, The Third Affiliated Hospital of Navy Medical University, Shanghai, China.

Funding

Biomedical Data Translator Technical Feasibility Assessment and Architecture DesignOT3TR002019 · NCATS · JOHNS HOPKINS UNIVERSITY · PI CHUTE, CHRISTOPHER G, HAENDEL, MELISSA A · 2016 to 2019
$5.7M
Laboratory Open Fund of Key Technology and Materials in Minimally Invasive Spine Surgery 2024JZWC-ZDB01National Natural Science Foundation of China 32200591National Natural Science Foundation of China 82272653NCATS NIH HHS OT3 TR002019Shanghai Pujiang Program 22PJD067The Talent Grant of Shanghai Tongren Hospital TR2019rc01
6 · The paper itself

Abstract

backgroundDCAF7/WDR68 (hereafter WDR68) is a highly conserved WD40 repeat protein across species and its role in mouse embryonic development is still unknown.

methodsThe mice deficient in WDR68 function by gene targeting were generated for its functional research. Several single-cell RNA-sequencing datasets that collectively span mouse gastrulation and organogenesis were integrated for reconstruction of expression trajectory of WDR68 spanning mouse embryogenesis. Weighted gene co-expression network analysis (WGCNA) was used for functional enrichment of co-expression genes of WDR68 in early embryos. Whole-embryo transcriptomic analyses were employed to reveal differentially expressed genes in WDR68-knockout mouse embryos. Co-immunoprecipitation in combination with liquid chromatography-mass spectrometry analysis was performed to examine the interacting proteins of WDR68.

resultsWDR68 null mutants exhibited intrauterine growth retardation (IUGR) and died during gestation. Mechanistically, WDR68 deficiency resulted in deregulated expression of development-related genes and activated Hypoxia-inducible factor-1 (HIF-1) pathway. The interactomics confirmed that WDR68 interacts with development-related proteins including AUTS2 and PCGF5.

conclusionsWDR68 is required for mouse embryonic development and may be a potential target for prevention and treatment of intrauterine growth retardation in the future.

Indexed as

Adaptor Proteins, Signal TransducingEmbryonic DevelopmentAnimalsEmbryo, MammalianFemaleGene Expression ProfilingGene Expression Regulation, DevelopmentalGene Regulatory NetworksMiceMice, KnockoutProtein BindingSignal TransductionAdaptor Proteins, Signal TransducingEmbryogenesisHIF-1Intrauterine growth retardationWDR68

Identifiers

PMID40462101
PMCPMC12135239

What OpenQuestion 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 OpenQuestion graph.