Evidence map›Paper›PMID 39907139›Full record

ReviewGenetics2025

Chaperone dysfunction in motor neuron disease: new insights from studies of the SMN complex.

A Gregory Matera

Abstract readReview
In one paragraph

Review in Genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Biomarkers in spinal muscular atrophy.Frontiers in neurology · 2025
    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

1 author.

A Gregory MateraIntegrative Program for Biological and Genome Sciences, University of North Carolina School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 25799, USA.ORCID 0000-0002-6406-0630

Funding

Role of histone PTMs in epigenetic control of metazoan transcription and RNA processingR35GM136435 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI A. Gregory Matera · 2020 to 2026
$4.7M
NIGMS NIH HHS R35 GM136435USA National Institutes of Health
6 · The paper itself

Abstract

Spinal muscular atrophy and amyotrophic lateral sclerosis are devastating neurodegenerative diseases characterized by motor neuron loss. Although these 2 disorders have distinct genetic origins, recent studies suggest that they share common etiological mechanisms rooted in proteostatic dysfunction. At the heart of this emerging understanding is the survival motor neuron (SMN) complex.

Indexed as

Molecular ChaperonesMotor Neuron DiseaseSMN Complex ProteinsAmyotrophic Lateral SclerosisAnimalsHumansMotor NeuronsMuscular Atrophy, SpinalMolecular ChaperonesSMN Complex ProteinsALSamyotrophic lateral sclerosisgenetic suppressorsheat shock proteinshspASMASMNspinal muscular atrophysurvival motor neuronTDP-43

Identifiers

PMID39907139
PMCPMC11912826

What OpenQuestion holds

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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.