Evidence map›Paper›PMID 26658019›Full record

ArticleCell death and differentiation2016

Cdk12 is essential for embryonic development and the maintenance of genomic stability.

H-C Juan, Y Lin, H-R Chen, M-J Fann

Abstract read
In one paragraph

Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing 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

65 citing papers in PubMed.

  1. Article
  2. Article
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  4. Article
  5. A Vertebrate Toxin-Antidote System That Sabotages Mouse Embryogenesis.bioRxiv : the preprint server for biology · 2026
    Article
  6. CDK12 and CDK13 in oncology: from RNA regulation to therapeutic targeting.Cellular oncology (Dordrecht, Netherlands) · 2026
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
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  15. Review
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  18. Article
  19. bioRxiv : the preprint server for biology · 2024
    Article
  20. Article

5 more citing papers are in PubMed but not listed here.

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.

H-C JuanDepartment of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei, Taiwan, Republic of China.
Y LinDepartment of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei, Taiwan, Republic of China.
H-R ChenDepartment of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei, Taiwan, Republic of China.
M-J FannDepartment of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei, Taiwan, Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The maintenance of genomic integrity during early embryonic development is important in order to ensure the proper development of the embryo. Studies from cultured cells have demonstrated that cyclin-dependent kinase 12 (Cdk12) is a multifunctional protein that maintains genomic stability and the pluripotency of embryonic stem cells. Perturbation of its functions is also known to be associated with pathogenesis and drug resistance in human cancers. However, the biological significance of Cdk12 in vivo is unclear. Here we bred mice that are deficient in Cdk12 and demonstrated that Cdk12 depletion leads to embryonic lethality shortly after implantation. We also used an in vitro culture system of blastocysts to examine the molecular mechanisms associated with the embryonic lethality of Cdk12-deficient embryos. Cdk12(-/-) blastocysts fail to undergo outgrowth of the inner cell mass because of an increase in the apoptosis of these cells. Spontaneous DNA damage was revealed by an increase in 53BP1 foci among cells cultured from Cdk12(-/-) embryos. Furthermore, the expression levels of various DNA damage response genes, namely Atr, Brca1, Fanci and Fancd2, are reduced in Cdk12(-/-) embryos. These findings indicate that Cdk12 is important for the correct expression of some DNA damage response genes and indirectly has an influence on the efficiency of DNA repair. Our report also highlights that DNA breaks occurring during DNA replication are frequent in mouse embryonic cells and repair of such damage is critical to the successful development of mouse embryos.

Indexed as

AnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsBlastocystBRCA1 ProteinCells, CulturedCyclin-Dependent KinasesDNA RepairEmbryonic DevelopmentFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group ProteinsGenomic InstabilityGenotypeMiceMice, Inbred C57BLMice, KnockoutAtaxia Telangiectasia Mutated ProteinsAtr protein, mouseBRCA1 ProteinCDK12 protein, mouseCyclin-Dependent KinasesFANCI protein, mouseFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group ProteinsOctamer Transcription Factor-3Pou5f1 protein, mouseTrp53bp1 protein, mouseTumor Suppressor p53-Binding Protein 1

Identifiers

PMID26658019
PMCPMC4987723

What OpenQuestion holds

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Registered trials

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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.