Evidence map›Paper›PMID 30443836›Full record

ArticleMarine biotechnology (New York, N.Y.)2019

Conditional Overexpression of rtn4al in Muscle of Adult Zebrafish Displays Defects Similar to Human Amyotrophic Lateral Sclerosis.

Cheng-Yung Lin, Po-Hsiang Zhang, You-Jei Chen, Chia-Lun Wu, Huai-Jen Tsai

Abstract read
PubMed Publisher
In one paragraph

Article in Marine biotechnology (New York, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. A 16-amino acid peptide delays the progression of motor neuron degeneration and pathogenic symptoms in ALS models.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. MicroRNAs in amyotrophic lateral sclerosis: from pathogenetic involvement to diagnostic biomarker and therapeutic agent development.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2020
    Review
  10. Article
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

5 authors at 2 institutions in 1 country.

Cheng-Yung LinInstitute of Biomedical Sciences, Mackay Medical College, No. 46, Sec. 3, Zhongzhen Road, Sanzhi Dist., New Taipei City, 252, Taiwan.
Po-Hsiang ZhangInstitute of Biomedical Sciences, Mackay Medical College, No. 46, Sec. 3, Zhongzhen Road, Sanzhi Dist., New Taipei City, 252, Taiwan.
You-Jei ChenInstitute of Molecular and Cellular Biology, National Taiwan University, No. 1, Section 4, Roosevelt Road, Taipei, 106, Taiwan.
Chia-Lun WuInstitute of Molecular and Cellular Biology, National Taiwan University, No. 1, Section 4, Roosevelt Road, Taipei, 106, Taiwan.
Huai-Jen TsaiInstitute of Biomedical Sciences, Mackay Medical College, No. 46, Sec. 3, Zhongzhen Road, Sanzhi Dist., New Taipei City, 252, Taiwan. hjtsai@ntu.edu.tw.
Mackay Medical College · TWNational Taiwan University · TW

Funding

Ministry of Science and Technology, Taiwan 104-2321-B-715-001
6 · The paper itself

Abstract

The protein level of muscle-specific human NogoA is abnormally upregulated in amyotrophic lateral sclerosis (ALS) mice and patients. On the other hand, while the presence of miR-206 in muscle cells delays onset and death in ALS, the relationship between these two phenomena remains unclear. Mammalian NogoA protein, also known as Reticulon 4a (Rtn4a), plays an important role in inhibiting the outgrowth of motor neurons. Our group previously identified zebrafish rtn4al as the target gene of miR-206 and found that knockdown of miR-206 increases rtn4al mRNA and Rtn4al protein in zebrafish embryos. It can be concluded from these results that neurite outgrowth of motor neurons is inhibited by Rtn4a1, which is entirely consistent with overexpression of either human NogoA or zebrafish homolog Rtn4al. Since an animal model able to express NogoA/rtn4al at the mature stage is unavailable, we generated a zebrafish transgenic line, Tg(Zα:TetON-Rtn4al), which conditionally and specifically overexpresses Rtn4al in the muscle tissue. After doxycycline induction, adult zebrafish displayed denervation at neuromuscular junction during the first week, then muscle disintegration and split myofibers during the third week, and, finally, significant weight loss in the sixth week. These results suggest that this zebrafish transgenic line, representing the inducible overexpression of Rtn4a1 in muscle, may provide an alternative animal model with which to study ALS because it exhibits ALS-like phenotype.

Indexed as

Disease Models, AnimalAmyotrophic Lateral SclerosisAnimalsAnimals, Genetically ModifiedDoxycyclineEmbryo, NonmammalianGene Expression RegulationHumansMicroRNAsMorpholinosMotor NeuronsMuscle, SkeletalMyelin ProteinsNeuromuscular JunctionNogo ProteinsOligonucleotides, AntisenseDoxycyclineMicroRNAsMIRN206 microRNA, humanMorpholinosMyelin ProteinsNogo ProteinsOligonucleotides, AntisenseRtn4a protein, zebrafishZebrafish ProteinsMotor neuronMuscleNogoARtn4alZebrafish

Identifiers

PMID30443836
OpenAlexW2901331591

What OpenQuestion holds

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Registered trials

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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.