Evidence map›Paper›PMID 31885126›Full record

ArticleEMBO reports2020

CEP41-mediated ciliary tubulin glutamylation drives angiogenesis through AURKA-dependent deciliation.

Soo Mi Ki, Ji Hyun Kim, So Yeon Won, Shin Ji Oh, In Young Lee, Young-Ki Bae, Ki Wha Chung, Byung-Ok Choi, Boyoun Park, Eui-Ju Choi and 1 more

Open access · hybridAbstract read
In one paragraph

Article in EMBO reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 41 citations in OpenAlex.

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  10. Post-Translational Modifications in Cilia and Ciliopathies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
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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

11 authors at 6 institutions in 1 country.

Soo Mi KiDepartment of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, South Korea.
Ji Hyun KimDepartment of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, South Korea.
So Yeon WonDepartment of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, South Korea.
Shin Ji OhDepartment of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, South Korea.
In Young LeeLaboratory of Cell Death and Human Diseases, Department of Life Sciences, Korea University, Seoul, South Korea.
Young-Ki BaeComparative Biomedicine Research & Tumor Microenvironment Research Branch, Research Institute, National Cancer Center, Goyang, Korea.
Ki Wha ChungDepartment of Biological Sciences, Kongju National University, Kongju, South Korea.
Byung-Ok ChoiDepartment of Neurology, Sungkyunkwan University School of Medicine, Seoul, South Korea.
Boyoun ParkDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, South Korea.
Eui-Ju ChoiLaboratory of Cell Death and Human Diseases, Department of Life Sciences, Korea University, Seoul, South Korea.
Ji Eun LeeDepartment of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, South Korea.ORCID 0000-0002-4898-741X
Sungkyunkwan University · KRKorea University · KRKongju National University · KRNational Cancer Center · KRSamsung Medical Center · KRYonsei University · KR

Funding

National Research Foundation of Korea (NRF) 2017R1E1A2A01076144National Research Foundation of Korea (NRF) 2018R1A2A3074597National Research Foundation of Korea (NRF) 2018R1A4A1024506National Research Foundation of Korea (NRF) NRF 2015041919
6 · The paper itself

Abstract

The endothelial cilium is a microtubule-based organelle responsible for blood flow-induced mechanosensation and signal transduction during angiogenesis. The precise function and mechanisms by which ciliary mechanosensation occurs, however, are poorly understood. Although posttranslational modifications (PTMs) of cytoplasmic tubulin are known to be important in angiogenesis, the specific roles of ciliary tubulin PTMs play remain unclear. Here, we report that loss of centrosomal protein 41 (CEP41) results in vascular impairment in human cell lines and zebrafish, implying a previously unknown pro-angiogenic role for CEP41. We show that proper control of tubulin glutamylation by CEP41 is necessary for cilia disassembly and that is involved in endothelial cell (EC) dynamics such as migration and tubulogenesis. We show that in ECs responding to shear stress or hypoxia, CEP41 activates Aurora kinase A (AURKA) and upregulates expression of VEGFA and VEGFR2 through ciliary tubulin glutamylation, as well as leads to the deciliation. We further show that in hypoxia-induced angiogenesis, CEP41 is responsible for the activation of HIF1α to trigger the AURKA-VEGF pathway. Overall, our results suggest the CEP41-HIF1α-AURKA-VEGF axis as a key molecular mechanism of angiogenesis and demonstrate how important ciliary tubulin glutamylation is in mechanosense-responded EC dynamics.

Indexed as

Aurora Kinase ATubulinAnimalsCiliaHumansMicrotubulesProteinsZebrafishAURKA protein, humanAurora Kinase ACEP41 protein, humanProteinsTubulinangiogenesisAURKACEP41primary ciliatubulin glutamylation

Identifiers

PMID31885126
PMCPMC7001496
OpenAlexW2997639730

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.