Evidence map›Paper›PMID 35301795›Full record

ArticleEMBO reports2022

ENKD1 promotes CP110 removal through competing with CEP97 to initiate ciliogenesis.

Ting Song, Yunfan Yang, Peng Zhou, Jie Ran, Liang Zhang, Xiaofan Wu, Wei Xie, Tao Zhong, Hongbin Liu, Min Liu and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

11 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. ENKD1 attenuates antibacterial immunity by facilitating TRIM21-mediated RUBCN degradation to suppress LC3-associated phagocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Formation and function of multiciliated cells.The Journal of cell biology · 2024
    Review
  10. Article
  11. 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

13 authors at 3 institutions in 1 country.

Ting Song *Shandong Provincial Key Laboratory of Animal Resistance Biology, Institute of Biomedical Sciences, College of Life Sciences, Collaborative Innovation Center of Cell Biology in Universities of Shandong, Shandong Normal University, Jinan, China.ORCID 0000-0001-5945-6676
Yunfan Yang *Cheeloo College of Medicine, Shandong University, Jinan, China.ORCID 0000-0002-5266-7208
Peng ZhouShandong Provincial Key Laboratory of Animal Resistance Biology, Institute of Biomedical Sciences, College of Life Sciences, Collaborative Innovation Center of Cell Biology in Universities of Shandong, Shandong Normal University, Jinan, China.
Jie RanShandong Provincial Key Laboratory of Animal Resistance Biology, Institute of Biomedical Sciences, College of Life Sciences, Collaborative Innovation Center of Cell Biology in Universities of Shandong, Shandong Normal University, Jinan, China.ORCID 0000-0002-0744-7126
Liang ZhangShandong Provincial Key Laboratory of Animal Resistance Biology, Institute of Biomedical Sciences, College of Life Sciences, Collaborative Innovation Center of Cell Biology in Universities of Shandong, Shandong Normal University, Jinan, China.
Xiaofan WuState Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecology, Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, China.
Wei XieShandong Provincial Key Laboratory of Animal Resistance Biology, Institute of Biomedical Sciences, College of Life Sciences, Collaborative Innovation Center of Cell Biology in Universities of Shandong, Shandong Normal University, Jinan, China.ORCID 0000-0002-3844-3013
Tao ZhongShandong Provincial Key Laboratory of Animal Resistance Biology, Institute of Biomedical Sciences, College of Life Sciences, Collaborative Innovation Center of Cell Biology in Universities of Shandong, Shandong Normal University, Jinan, China.ORCID 0000-0003-3898-057X
Hongbin LiuCheeloo College of Medicine, Shandong University, Jinan, China.ORCID 0000-0003-2550-7492
Min LiuShandong Provincial Key Laboratory of Animal Resistance Biology, Institute of Biomedical Sciences, College of Life Sciences, Collaborative Innovation Center of Cell Biology in Universities of Shandong, Shandong Normal University, Jinan, China.
Dengwen LiState Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecology, Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, China.
Huijie ZhaoShandong Provincial Key Laboratory of Animal Resistance Biology, Institute of Biomedical Sciences, College of Life Sciences, Collaborative Innovation Center of Cell Biology in Universities of Shandong, Shandong Normal University, Jinan, China.ORCID 0000-0002-8595-8159
Jun ZhouShandong Provincial Key Laboratory of Animal Resistance Biology, Institute of Biomedical Sciences, College of Life Sciences, Collaborative Innovation Center of Cell Biology in Universities of Shandong, Shandong Normal University, Jinan, China.ORCID 0000-0003-3131-7804
Shandong Normal University · CNNankai University · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the importance of cilia in cell signaling and motility, the molecular mechanisms regulating cilium formation remain incompletely understood. Herein, we characterize enkurin domain-containing protein 1 (ENKD1) as a novel centrosomal protein that mediates the removal of centriolar coiled-coil protein 110 (CP110) from the mother centriole to promote ciliogenesis. We show that Enkd1 knockout mice possess ciliogenesis defects in multiple organs. Super-resolution microscopy reveals that ENKD1 is a stable component of the centrosome throughout the ciliogenesis process. Simultaneous knockdown of ENKD1 and CP110 significantly reverses the ciliogenesis defects induced by ENKD1 depletion. Protein interaction analysis shows that ENKD1 competes with centrosomal protein 97 (CEP97) in binding to CP110. Depletion of ENKD1 enhances the CP110-CEP97 interaction and detains CP110 at the mother centriole. These findings thus identify ENKD1 as a centrosomal protein and uncover a novel mechanism controlling CP110 removal from the mother centriole for the initiation of ciliogenesis.

Indexed as

CentriolesMicrotubule-Associated ProteinsAnimalsCalmodulin-Binding ProteinsCell Cycle ProteinsCentrosomeCiliaMiceMicrotubule ProteinsSeminal Plasma ProteinsCalmodulin-Binding ProteinsCcp110 protein, MouseCell Cycle ProteinsCEP97 protein, mouseEnkd1 protein, mouseenkurin protein, mouseMicrotubule-Associated ProteinsMicrotubule ProteinsSeminal Plasma ProteinscentrosomeciliogenesisciliumCP110ENKD1

Identifiers

PMID35301795
PMCPMC9066061
OpenAlexW4220653445

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.