Evidence map›Paper›PMID 24797473›Full record

ArticleThe EMBO journal2014

ICK is essential for cell type-specific ciliogenesis and the regulation of ciliary transport.

Taro Chaya, Yoshihiro Omori, Ryusuke Kuwahara, Takahisa Furukawa

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
5.8field-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

84 citing papers in PubMed, 120 citations in OpenAlex.

  1. Review
  2. Article
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  6. Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Review
  8. Article
  9. Article
  10. Post-Translational Modifications in Cilia and Ciliopathies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  11. Article
  12. Review
  13. Article
  14. The intraflagellar transport cycle.Nature reviews. Molecular cell biology · 2025
    Review
  15. Article
  16. Mechanism and regulation of kinesin motors.Nature reviews. Molecular cell biology · 2025
    Review
  17. Review
  18. Article
  19. Article
  20. Article

24 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 at 2 institutions in 1 country.

Taro ChayaLaboratory for Molecular and Developmental Biology, Institute for Protein Research Osaka University, Suita Osaka, Japan JST CREST, Suita Osaka, Japan Department of Developmental Biology, Osaka Bioscience Institute, Suita Osaka, Japan Kyoto University Graduate School of Medicine, Sakyo-ku Kyoto, Japan.
Yoshihiro OmoriLaboratory for Molecular and Developmental Biology, Institute for Protein Research Osaka University, Suita Osaka, Japan JST CREST, Suita Osaka, Japan Department of Developmental Biology, Osaka Bioscience Institute, Suita Osaka, Japan JST PRESTO, Suita Osaka, Japan.
Ryusuke KuwaharaResearch Center for Ultrahigh Voltage Electron Microscopy Osaka University, Ibaraki Osaka, Japan.
Takahisa FurukawaLaboratory for Molecular and Developmental Biology, Institute for Protein Research Osaka University, Suita Osaka, Japan JST CREST, Suita Osaka, Japan Department of Developmental Biology, Osaka Bioscience Institute, Suita Osaka, Japan takahisa.furukawa@protein.osaka-u.ac.jp.
Protein Research Foundation · JPOsaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cilia and flagella are formed and maintained by intraflagellar transport (IFT) and play important roles in sensing and moving across species. At the distal tip of the cilia/flagella, IFT complexes turn around to switch from anterograde to retrograde transport; however, the underlying regulatory mechanism is unclear. Here, we identified ICK localization at the tip of cilia as a regulator of ciliary transport. In ICK-deficient mice, we found ciliary defects in neuronal progenitor cells with Hedgehog signal defects. ICK-deficient cells formed cilia with mislocalized Hedgehog signaling components. Loss of ICK caused the accumulation of IFT-A, IFT-B, and BBSome components at the ciliary tips. In contrast, overexpression of ICK induced the strong accumulation of IFT-B, but not IFT-A or BBSome components at ciliary tips. In addition, ICK directly phosphorylated Kif3a, while inhibition of this Kif3a phosphorylation affected ciliary formation. Our results suggest that ICK is a Kif3a kinase and essential for proper ciliogenesis in development by regulating ciliary transport at the tip of cilia.

Indexed as

AnimalsBiological TransportBrainCiliaFemaleFlagellaHedgehog ProteinsKinesinsLungMaleMiceMice, Inbred C57BLMice, KnockoutMicrotubule-Associated ProteinsMutationNeuronsHedgehog ProteinsKif3a protein, mouseKinesinsMicrotubule-Associated ProteinsProtein Serine-Threonine Kinasesciliary transportciliogenesiskinasekinesin

Identifiers

PMID24797473
PMCPMC4198026
OpenAlexW2134281520

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.