Evidence map›Paper›PMID 25270598›Full record

ArticleNature communications2014

Ubiquitin-proteasome system controls ciliogenesis at the initial step of axoneme extension.

Kousuke Kasahara, Yoshitaka Kawakami, Tohru Kiyono, Shigenobu Yonemura, Yoshifumi Kawamura, Saho Era, Fumio Matsuzaki, Naoki Goshima, Masaki Inagaki

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
9.1field-weighted citation impact, top 2% 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

87 citing papers in PubMed, 131 citations in OpenAlex.

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  7. KCTD1 regulation of Adenylyl cyclase type 5 adjusts striatal cAMP signaling.Proceedings of the National Academy of Sciences of the United States of America · 2024
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27 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

9 authors at 5 institutions in 1 country.

Kousuke Kasahara1] Division of Biochemistry, Aichi Cancer Center Research Institute, Nagoya, Aichi 464-8681, Japan [2] Department of Oncology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Aichi 467-8603, Japan.
Yoshitaka KawakamiMolecular Profiling Research Center for Drug Discovery, National Institute of Advanced Industrial Science and Technology, Tokyo 135-0064, Japan.
Tohru KiyonoVirology Division, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Shigenobu YonemuraElectron Microscope Laboratory, RIKEN Center for Developmental Biology, Kobe 650-0047, Japan.
Yoshifumi KawamuraJapan Biological Informatics Consortium (JBiC), Tokyo 135-8073, Japan.
Saho EraDivision of Biochemistry, Aichi Cancer Center Research Institute, Nagoya, Aichi 464-8681, Japan.
Fumio MatsuzakiLaboratory of Cell Asymmetry, RIKEN Center of Developmental Biology, Kobe 650-0047, Japan.
Naoki GoshimaMolecular Profiling Research Center for Drug Discovery, National Institute of Advanced Industrial Science and Technology, Tokyo 135-0064, Japan.
Masaki Inagaki1] Division of Biochemistry, Aichi Cancer Center Research Institute, Nagoya, Aichi 464-8681, Japan [2] Department of Cellular Oncology, Nagoya University Graduate School of Medicine, Nagoya, Aichi 466-8550, Japan.
Aichi Cancer Center · JPNational Institute of Advanced Industrial Science and Technology · JPRIKEN Center for Computational Science · JPJapan Biological Informatics Consortium · JPNagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary cilia are microtubule-based sensory organelles that organize numerous key signals during developments and tissue homeostasis. Ciliary microtubule doublet, named axoneme, is grown directly from the distal end of mother centrioles through a multistep process upon cell cycle exit; however, the instructive signals that initiate these events are poorly understood. Here we show that ubiquitin-proteasome machinery removes trichoplein, a negative regulator of ciliogenesis, from mother centrioles and thereby causes Aurora-A inactivation, leading to ciliogenesis. Ciliogenesis is blocked if centriolar trichoplein is stabilized by treatment with proteasome inhibitors or by expression of non-ubiquitylatable trichoplein mutant (K50/57R). Started from two-stepped global E3 screening, we have identified KCTD17 as a substrate-adaptor for Cul3-RING E3 ligases (CRL3s) that polyubiquitylates trichoplein. Depletion of KCTD17 specifically arrests ciliogenesis at the initial step of axoneme extension through aberrant trichoplein-Aurora-A activity. Thus, CRL3-KCTD17 targets trichoplein to proteolysis to initiate the axoneme extension during ciliogenesis.

Indexed as

Adaptor Proteins, Signal TransducingAxonemeCentriolesCiliaCullin ProteinsHumansProteasome Endopeptidase ComplexUbiquitinAdaptor Proteins, Signal TransducingCUL3 protein, humanCullin ProteinsKCTD17 protein, humanProteasome Endopeptidase ComplexUbiquitin

Identifiers

PMID25270598
PMCPMC4205846
OpenAlexW1987768246

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.