Evidence map›Paper›PMID 36320323›Full record

ArticleMolecular therapy. Nucleic acids2022

miR-196a enhances polymerization of neuronal microfilaments through suppressing IMP3 and upregulating IGF2 in Huntington's disease.

Han-In Yang, Pin-Yu Huang, Siew Chin Chan, Chih-Wei Tung, Pei-Hsun Cheng, Chuan-Mu Chen, Shang-Hsun Yang

Abstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

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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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Rad23b exacerbates pathological aggregates through disrupting proteasome functions in Spinocerebellar ataxia type 3.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  4. Article
  5. 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

7 authors.

Han-In YangDepartment of Physiology, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
Pin-Yu HuangDepartment of Physiology, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
Siew Chin ChanDepartment of Physiology, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
Chih-Wei TungDepartment of Physiology, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
Pei-Hsun ChengDepartment of Physiology, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
Chuan-Mu ChenDepartment of Life Sciences, College of Life Sciences, National Chung Hsing University, Taichung 40227, Taiwan.
Shang-Hsun YangDepartment of Physiology, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Huntington's disease (HD) is one of the inheritable neurodegenerative diseases, and these diseases share several similar pathological characteristics, such as abnormal neuronal morphology. miR-196a is a potential target to provide neuroprotective functions, and has been reported to enhance polymerization of neuronal microtubules in HD. While microtubules and microfilaments are two important components of the neuronal cytoskeleton, whether miR-196a improves neuronal microfilaments is still unknown. Here, we identify insulin-like growth factor 2 mRNA binding protein 3 (IMP3), and show that miR-196a directly suppresses IMP3 to increase neurite outgrowth in neurons. In addition, IMP3 disturbs neurite outgrowth

Indexed as

Huntington’s diseaseIGF2IMP3microfilamentmiR-196aMT: Non-coding RNAsneurite outgrowth

Identifiers

PMID36320323
PMCPMC9593307

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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.