Evidence map›Paper›PMID 28701747›Full record

ArticleScientific reports2017

NEAP/DUSP26 suppresses receptor tyrosine kinases and regulates neuronal development in zebrafish.

Chi-Hwa Yang, Yu-Jung Yeh, Jiz-Yuh Wang, Ya-Wen Liu, Yen-Lin Chen, Hui-Wen Cheng, Chun-Mei Cheng, Yung-Jen Chuang, Chiou-Hwa Yuh, Yi-Rong Chen

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  5. Review
  6. Article
  7. A Review of DUSP26: Structure, Regulation and Relevance in Human Disease.International journal of molecular sciences · 2021
    Review
  8. Article
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  10. 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

10 authors at 3 institutions in 1 country.

Chi-Hwa YangInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, 350, Taiwan.
Yu-Jung YehInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, 350, Taiwan.
Jiz-Yuh WangInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, 350, Taiwan.
Ya-Wen LiuInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, 350, Taiwan.
Yen-Lin ChenInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, 350, Taiwan.
Hui-Wen ChengInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, 350, Taiwan.
Chun-Mei ChengInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, 350, Taiwan.
Yung-Jen ChuangInstitute of Bioinformatics and Structural Biology, National Tsing Hua University, Hsinchu, 300, Taiwan.ORCID 0000-0002-6022-0107
Chiou-Hwa YuhInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, 350, Taiwan.
Yi-Rong ChenInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, 350, Taiwan. yrchen@nhri.org.tw.
National Health Research Institutes · TWKaohsiung Medical University · TWNational Tsing Hua University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Expression of neuroendocrine-associated phosphatase (NEAP, also named as dual specificity phosphatase 26, [DUSP26]) is restricted to neuroendocrine tissues. We found that NEAP, but not its phosphatase-defective mutant, suppressed nerve growth factor (NGF) receptor TrkA and fibroblast growth factor receptor 1 (FGFR1) activation in PC12 cells upon NGF stimulation. Conversely, suppressing NEAP expression by RNA interference enhanced TrkA and FGFR1 phosphorylation. NEAP was capable of de-phosphorylating TrkA and FGFR1 directly in vitro. NEAP-orthologous gene existed in zebrafish. Morpholino (MO) suppression of NEAP in zebrafish resulted in hyper-phosphorylation of TrkA and FGFR1 as well as abnormal body postures and small eyes. Differentiation of retina in zebrafishes with NEAP MO treatment was severely defective, so were cranial motor neurons. Taken together, our data indicated that NEAP/DUSP26 have a critical role in regulating TrkA and FGFR1 signaling as well as proper development of retina and neuronal system in zebrafish.

Indexed as

AnimalsCell DifferentiationDual-Specificity PhosphatasesEmbryo, NonmammalianMitogen-Activated Protein Kinase PhosphatasesMorpholinosMotor Neuron DiseasePC12 CellsPhosphorylationRatsReceptor, Fibroblast Growth Factor, Type 1Receptor, trkARetinal DiseasesSignal TransductionZebrafishZebrafish ProteinsDual-Specificity PhosphatasesDUSP26 protein, zebrafishMitogen-Activated Protein Kinase PhosphatasesMorpholinosReceptor, Fibroblast Growth Factor, Type 1Receptor, trkAZebrafish Proteins

Identifiers

PMID28701747
PMCPMC5507855
OpenAlexW2733617798

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.