Evidence map›Paper›PMID 36799225›Full record

ArticleZoological research2023

C9orf72 poly-GA proteins impair neuromuscular transmission.

Wen-Yo Tu, Wentao Xu, Jianmin Zhang, Shuyuan Qi, Lei Bai, Chengyong Shen, Kejing Zhang

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Zoological research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 18% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
  2. Targeting GeneInternational journal of molecular sciences · 2025
    Review
  3. The MuSK agonist antibody protects the neuromuscular junction and extends the lifespan in C9orf72-ALS mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  4. Aberrant evoked calcium signaling and nAChR cluster morphology in aFrontiers in cell and developmental biology · 2024
    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 at 2 institutions in 1 country.

Wen-Yo TuZhejiang Provincial Key Laboratory of Pancreatic Disease, Department of Neurobiology, First Affiliated Hospital, Institute of Translational Medicine, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310020, China.
Wentao XuZhejiang Provincial Key Laboratory of Pancreatic Disease, Department of Neurobiology, First Affiliated Hospital, Institute of Translational Medicine, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310020, China.
Jianmin ZhangZhejiang Provincial Key Laboratory of Pancreatic Disease, Department of Neurobiology, First Affiliated Hospital, Institute of Translational Medicine, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310020, China.
Shuyuan QiZhejiang Provincial Key Laboratory of Pancreatic Disease, Department of Neurobiology, First Affiliated Hospital, Institute of Translational Medicine, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310020, China.
Lei BaiZhejiang Provincial Key Laboratory of Pancreatic Disease, Department of Neurobiology, First Affiliated Hospital, Institute of Translational Medicine, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310020, China.
Chengyong ShenZhejiang Provincial Key Laboratory of Pancreatic Disease, Department of Neurobiology, First Affiliated Hospital, Institute of Translational Medicine, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310020, China.
Kejing ZhangZhejiang Provincial Key Laboratory of Pancreatic Disease, Department of Neurobiology, First Affiliated Hospital, Institute of Translational Medicine, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310020, China. E-mail: kjzhang@zju.edu.cn.
First Affiliated Hospital Zhejiang University · CNZhejiang Lab · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a devastating motoneuron disease, in which lower motoneurons lose control of skeletal muscles. Degeneration of neuromuscular junctions (NMJs) occurs at the initial stage of ALS. Dipeptide repeat proteins (DPRs) from G4C2 repeat-associated non-ATG (RAN) translation are known to cause C9orf72-associated ALS (C9-ALS). However, DPR inclusion burdens are weakly correlated with neurodegenerative areas in C9-ALS patients, indicating that DPRs may exert cell non-autonomous effects, in addition to the known intracellular pathological mechanisms. Here, we report that poly-GA, the most abundant form of DPR in C9-ALS, is released from cells. Local administration of poly-GA proteins in peripheral synaptic regions causes muscle weakness and impaired neuromuscular transmission

Indexed as

Amyotrophic Lateral SclerosisAgrinAnimalsC9orf72 ProteinDipeptidesDisease Models, AnimalAgrinC9orf72 ProteinDipeptidesAgrinAmyotrophic lateral sclerosisNeuromuscular junctionPoly-Gly-Ala

Identifiers

PMID36799225
PMCPMC10083233
OpenAlexW4321172463

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.