Evidence map›Paper›PMID 31938364›Full record

ArticleInternational journal of clinical and experimental pathology2018

Activation of β-catenin causes defects in embryonic development during maternal-to-zygotic transition in mice.

Jun Yu, Xueke Guo, Xia Chen, Chen Qiao, Binghai Chen, Bing Xie, Xiaojin Luan, Cong Shen, Jiawei Zhu, Jiajia Liu and 5 more

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 49% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
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

15 authors at 3 institutions in 1 country.

Jun YuDepartment of Gynecology, Affiliated Hospital of Jiangsu University, Jiangsu University Zhenjiang 212001, Jiangsu, China.
Xueke GuoDepartment of Gynecology, Affiliated Hospital of Jiangsu University, Jiangsu University Zhenjiang 212001, Jiangsu, China.
Xia ChenDepartment of Gynecology, Affiliated Hospital of Jiangsu University, Jiangsu University Zhenjiang 212001, Jiangsu, China.
Chen QiaoDepartment of Clinical Pharmacy, Affiliated Hospital of Jiangsu University, Jiangsu University Zhenjiang 212001, Jiangsu, China.
Binghai ChenDepartment of Urology, Affiliated Hospital of Jiangsu University, Jiangsu University Zhenjiang 212001, Jiangsu, China.
Bing XieDepartment of Gynecology, Affiliated Hospital of Jiangsu University, Jiangsu University Zhenjiang 212001, Jiangsu, China.
Xiaojin LuanDepartment of Gynecology, Affiliated Hospital of Jiangsu University, Jiangsu University Zhenjiang 212001, Jiangsu, China.
Cong ShenCenter for Reproduction and Genetics, Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University Suzhou 215002, China.
Jiawei ZhuCenter for Reproduction and Genetics, Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University Suzhou 215002, China.
Jiajia LiuDepartment of Gynecology, Affiliated Hospital of Jiangsu University, Jiangsu University Zhenjiang 212001, Jiangsu, China.
Yidan YanDepartment of Gynecology, Affiliated Hospital of Jiangsu University, Jiangsu University Zhenjiang 212001, Jiangsu, China.
Zeyu HeDepartment of Clinical Medicine, China Medical University Shenyang, Liaoning, China.
Bo ZhengCenter for Reproduction and Genetics, Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University Suzhou 215002, China.
Hong LiCenter for Reproduction and Genetics, Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University Suzhou 215002, China.
Jie FangDepartment of Gynecology, Affiliated Hospital of Jiangsu University, Jiangsu University Zhenjiang 212001, Jiangsu, China.
Jiangsu University · CNSuzhou Municipal Hospital · CNChina Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The early stage of embryogenesis is an important and complex cell-remodeling event in reproductive biology. To develop into a normal zygote, maternal-to-zygotic transition (MZT) is especially important for both zygotic genome activation (ZGA) and degradation of maternal products during the early stage of embryonic development. β-Catenin has been identified as an important regulator of embryonic development and adult stem cell division via the canonical Wnt/β-catenin signalling pathway. However, the role of activated β-catenin during MZT remains elusive. In the present study, we found that β-catenin is mainly expressed during embryogenesis in the cell membrane from the zygote- to morula-stage embryos but not in MII oocytes. To analyze the function of activated β-catenin during MZT, we conducted a β-catenin activation assay during embryogenesis. Our results indicated that development beyond the two-cell stage was inhibited in zygotes with β-catenin activation. Further analysis showed that activated form of β-catenin protein was increased and the phosphorylated form of β-catenin protein was decreased in culture embryos. Taken together, our study reveals that activation of β-catenin may play a vital role in zygotic development, determining the developmental potential of mouse embryos.

Indexed as

embryonic developmentmaternal-to-zygotic transitionSKL2001two-cell stage blockβ-catenin

Identifiers

PMID31938364
PMCPMC6958268
OpenAlexW3028284890

What OpenQuestion holds

Textmetadata
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.