Evidence map›Paper›PMID 26880200›Full record

ArticleThe Journal of cell biology2016

Ndel1 suppresses ciliogenesis in proliferating cells by regulating the trichoplein-Aurora A pathway.

Hironori Inaba, Hidemasa Goto, Kousuke Kasahara, Kanako Kumamoto, Shigenobu Yonemura, Akihito Inoko, Shotaro Yamano, Hideki Wanibuchi, Dongwei He, Naoki Goshima and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
8.4field-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

51 citing papers in PubMed, 73 citations in OpenAlex.

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  20. The emerging role of the KCTD proteins in cancer.Cell communication and signaling : CCS · 2021
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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 5 institutions in 1 country.

Hironori InabaDivision of Biochemistry, Aichi Cancer Center Research Institute, Nagoya 464-8681, Japan.
Hidemasa GotoDivision of Biochemistry, Aichi Cancer Center Research Institute, Nagoya 464-8681, Japan Department of Cellular Oncology, Graduate School of Medicine, Nagoya University, Nagoya 466-8550, Japan.
Kousuke KasaharaDivision of Biochemistry, Aichi Cancer Center Research Institute, Nagoya 464-8681, Japan Department of Oncology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya 467-8601, Japan.
Kanako KumamotoDepartment of Genetic Disease Research, Osaka City University Graduate School of Medicine, Osaka 545-8585, Japan.
Shigenobu YonemuraCenter for Life Science Technologies (Ultrastructural Research Team), Institute of Physical and Chemical Research, Kobe 650-0047, Japan.
Akihito InokoDivision of Biochemistry, Aichi Cancer Center Research Institute, Nagoya 464-8681, Japan.
Shotaro YamanoDepartment of Molecular Pathology, Osaka City University Graduate School of Medicine, Osaka 545-8585, Japan.
Hideki WanibuchiDepartment of Molecular Pathology, Osaka City University Graduate School of Medicine, Osaka 545-8585, Japan.
Dongwei HeDivision of Biochemistry, Aichi Cancer Center Research Institute, Nagoya 464-8681, Japan.
Naoki GoshimaMolecular Profiling Research Center for Drug Discovery, National Institute of Advanced Industrial Science and Technology, Tokyo 135-0064, Japan.
Tohru KiyonoDivision of Carcinogenesis and Cancer Prevention, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Shinji HirotsuneDepartment of Genetic Disease Research, Osaka City University Graduate School of Medicine, Osaka 545-8585, Japan.
Masaki InagakiDivision of Biochemistry, Aichi Cancer Center Research Institute, Nagoya 464-8681, Japan Department of Cellular Oncology, Graduate School of Medicine, Nagoya University, Nagoya 466-8550, Japan minagaki@aichi-cc.jp.
Aichi Cancer Center · JPOsaka City University · JPGenesis Research Institute · JPNagoya City University · JPNational Institute of Advanced Industrial Science and Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary cilia protrude from the surface of quiescent cells and disassemble at cell cycle reentry. We previously showed that ciliary reassembly is suppressed by trichoplein-mediated Aurora A activation pathway in growing cells. Here, we report that Ndel1, a well-known modulator of dynein activity, localizes at the subdistal appendage of the mother centriole, which nucleates a primary cilium. In the presence of serum, Ndel1 depletion reduces trichoplein at the mother centriole and induces unscheduled primary cilia formation, which is reverted by forced trichoplein expression or coknockdown of KCTD17 (an E3 ligase component protein for trichoplein). Serum starvation induced transient Ndel1 degradation, subsequent to the disappearance of trichoplein at the mother centriole. Forced expression of Ndel1 suppressed trichoplein degradation and axonemal microtubule extension during ciliogenesis, similar to trichoplein induction or KCTD17 knockdown. Most importantly, the proportion of ciliated and quiescent cells was increased in the kidney tubular epithelia of newborn Ndel1-hypomorphic mice. Thus, Ndel1 acts as a novel upstream regulator of the trichoplein-Aurora A pathway to inhibit primary cilia assembly.

Indexed as

Cell ProliferationSignal TransductionAdaptor Proteins, Signal TransducingAnimalsAnimals, NewbornAurora Kinase ACarrier ProteinsCell Cycle CheckpointsCentriolesCiliaEpithelial CellsGenotypeHeLa CellsHumansKidney TubulesMiceAdaptor Proteins, Signal TransducingAURKA protein, humanAurka protein, mouseAurora Kinase ACarrier ProteinsKCTD17 protein, humanNDEL1 protein, humanNdel1 protein, mouseTCHP protein, human

Identifiers

PMID26880200
PMCPMC4754717
OpenAlexW2277747528

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.