Evidence map›Paper›PMID 29115376›Full record

ArticleInternational journal of molecular medicine2018

CCDC134 serves a crucial role in embryonic development.

Biaoyi Yu, Tianzhuo Zhang, Peng Xia, Xiaoting Gong, Xiaoyan Qiu, Jing Huang

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. ER-resident CCDC134 safeguards TLR4 maturation by maintaining gp96 stability.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
  6. CCDC134 controls TLR biogenesis through the ER chaperone Gp96.The Journal of experimental medicine · 2025
    Article
  7. Update on the Genetics of Osteogenesis Imperfecta.Calcified tissue international · 2024
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. 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

6 authors at 1 institution in 1 country.

Biaoyi YuDepartment of Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, P.R. China.
Tianzhuo ZhangDepartment of Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, P.R. China.
Peng XiaDepartment of Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, P.R. China.
Xiaoting GongDepartment of Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, P.R. China.
Xiaoyan QiuDepartment of Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, P.R. China.
Jing HuangDepartment of Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, P.R. China.
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coiled-coil domain containing 134 (CCDC134), a characterized secreted protein, may serve as an immune cytokine and illustrates its potent antitumor effects by augmenting CD8+ T-cell-mediated immunity. Additionally, CCDC134 may also act as a novel regulator of human alteration/deficiency in activation 2a, and be involved in the p300-CBP-associated factor complex and affect its acetyltransferase activity. To clarify the biological and pathological function of CCDC134, the present study generated a viable and fertile Ccdc134fl/fl mouse strain that allowed temporal and spatial control of gene ablation. Ccdc134-/- embryos generated by crossing of Ccdc134fl/fl mice with human β-actin-Cre or zona pellucida 3-Cre transgenic mice were embryonic lethal from embryonic day (E)12.5 to birth. Ccdc134 loss was associated with severe hemorrhages in the brain ventricular space and neural tube, pale and abnormal livers, cardiac hypertrophy and placental distress. Furthermore, it was demonstrated that a fraction of E13.5 fetal livers and brains exhibited reduced cell proliferation and vascular endothelial cell defects. CCDC134 also exhibited a dynamic and specific expression pattern during embryo development. The present results suggest that Ccdc134 may have specific biological functions in regulating mouse embryonic development.

Indexed as

AnimalsCell ProliferationEmbryonic DevelopmentFemaleGene Expression Regulation, DevelopmentalHumansIntracranial HemorrhagesLiverMembrane ProteinsMiceMice, TransgenicPregnancyCCDC134 protein, humanMembrane Proteins

Identifiers

PMID29115376
PMCPMC5746300
OpenAlexW2767019634

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.