Evidence map›Paper›PMID 32914523›Full record

ArticleCell proliferation2020

CHK1 monitors spindle assembly checkpoint and DNA damage repair during the first cleavage of mouse early embryos.

Jia-Qian Ju, Xiao-Han Li, Meng-Hao Pan, Yao Xu, Ming-Hong Sun, Yi Xu, Shao-Chen Sun

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Chromatin Modifier EP400 Regulates Oocyte Quality and Zygotic Genome Activation in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  3. Article
  4. Review
  5. Review
  6. Safeguarding DNA Replication: A Golden Touch of MiDAS and Other Mechanisms.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Review
  9. Article
  10. 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

7 authors at 1 institution in 1 country.

Jia-Qian JuCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China.
Xiao-Han LiCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China.
Meng-Hao PanCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China.
Yao XuCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China.
Ming-Hong SunCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China.
Yi XuCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China.
Shao-Chen SunCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China.ORCID https://orcid.org/0000-0001-5060-1742
Nanjing Agricultural University · CN

Funding

Fundamental Research Funds for the Central Universities, China KJYQ201701National Key Research and Development Program 2018YFC1003802National Key Research and Development Program 2018YFC1004003
6 · The paper itself

Abstract

objectivesDNA damage and errors of accurate chromosome segregation lead to aneuploidy and foetal defects. DNA repair and the spindle assembly checkpoint (SAC) are the mechanisms developed to protect from these defects. Checkpoint kinase 1 (CHK1) is reported to be an important DNA damage response protein in multiple models, but its functions remain unclear in early mouse embryos. MATERIALS AND

methodsImmunofluorescence staining, immunoblotting and real-time reverse transcription polymerase chain reaction were used to perform the analyses. Reactive oxygen species levels and Annexin-V were also detected.

resultsLoss of CHK1 activity accelerated progress of the cell cycle at the first cleavage; however, it disturbed the development of early embryos to the morula/blastocyst stages. Further analysis indicated that CHK1 participated in spindle assembly and chromosome alignment, possibly due to its regulation of kinetochore-microtubule attachment and recruitment of BubR1 and p-Aurora B to the kinetochores, indicating its role in SAC activity. Loss of CHK1 activity led to embryonic DNA damage and oxidative stress, which further induced early apoptosis and autophagy, indicating that CHK1 is responsible for interphase DNA damage repair.

conclusionsOur results indicate that CHK1 is a key regulator of the SAC and DNA damage repair during early embryonic development in mice.

Indexed as

DNA RepairM Phase Cell Cycle CheckpointsAnimalsApoptosisAurora Kinase BCell Cycle ProteinsCheckpoint Kinase 1Chromosome SegregationDNA DamageEmbryo, MammalianEmbryonic DevelopmentKinetochoresMiceMicrotubulesOxidative StressPhenylurea CompoundsAurora Kinase BBub1b protein, mouseCell Cycle ProteinsCheckpoint Kinase 1LY2603618Phenylurea CompoundsProtein Serine-Threonine KinasesPyrazinesReactive Oxygen Species

Identifiers

PMID32914523
PMCPMC7574881
OpenAlexW3086368870

What OpenQuestion 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 OpenQuestion graph.