Evidence map›Paper›PMID 33277610›Full record

ArticleScientific reports2020

Coiled-coil domain containing 50-V2 protein positively regulates neurite outgrowth.

Ju-Sik Min, Debasish Halder, Ji-Yong Yoon, Su-Jin Jeon, Soo Young Jun, Jae-Ran Lee, Jeong-Ju Lee, Min-Hyuk Choi, Cho-Rok Jung, DaYong Lee and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 49% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Review
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

12 authors at 3 institutions in 1 country.

Ju-Sik MinRare Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.
Debasish HalderRare Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.
Ji-Yong YoonRare Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.
Su-Jin JeonRare Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.
Soo Young JunRare Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.
Jae-Ran LeeRare Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.ORCID 0000-0002-4634-8489
Jeong-Ju LeeRare Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.
Min-Hyuk ChoiRare Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.
Cho-Rok JungRare Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.
DaYong LeeRare Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.
Byoung-Joon KimDepartment of Neurology, Sungkyunkwan University School of Medicine, Samsung Medical Center, Gangnam-gu, Seoul, 06351, Republic of Korea.
Nam-Soon KimRare Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea. nskim37@kribb.re.kr.
Korea Research Institute of Bioscience and Biotechnology · KRDaegu-Gyeongbuk Medical Innovation Foundation · KRSamsung Medical Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The coiled-coil domain containing 50 (CCDC50) protein is a phosphotyrosine-dependent signalling protein stimulated by epidermal growth factor. It is highly expressed in neuronal cells in the central nervous system; however, the roles of CCDC50 in neuronal development are largely unknown. In this study, we showed that the depletion of CCDC50-V2 impeded the neuronal development process, including arbor formation, spine density development, and axonal outgrowth, in primary neurons. Mechanistic studies revealed that CCDC50-V2 positively regulated the nerve growth factor receptor, while it downregulated the epidermal growth factor receptor pathway. Importantly, JNK/c-Jun activation was found to be induced by the CCDC50-V2 overexpression, in which the interaction between CCDC50-V2 and JNK2 was also observed. Overall, the present study demonstrates a novel mechanism of CCDC50 function in neuronal development and provides new insight into the link between CCDC50 function and the aetiology of neurological disorders.

Indexed as

Neuronal OutgrowthAnimalsCell Line, TumorErbB ReceptorsHEK293 CellsHumansIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesMiceNerve Tissue ProteinsProto-Oncogene Proteins c-junReceptors, Nerve Growth FactorSignal TransductionCCDC50 protein, humanEGFR protein, humanErbB ReceptorsIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesNerve Tissue ProteinsNGFR protein, humanProto-Oncogene Proteins c-junReceptors, Nerve Growth Factor

Identifiers

PMID33277610
PMCPMC7718278
OpenAlexW3107243454

What OpenQuestion holds

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LicenceCC BY
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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.