Evidence map›Paper›PMID 25246652›Full record

ArticleRNA (New York, N.Y.)2014

Subcellular transcriptome alterations in a cell culture model of spinal muscular atrophy point to widespread defects in axonal growth and presynaptic differentiation.

Lena Saal, Michael Briese, Susanne Kneitz, Michael Glinka, Michael Sendtner

Open access · bronzeAbstract read
In one paragraph

Article in RNA (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

66 citing papers in PubMed, 94 citations in OpenAlex.

  1. Synaptic Proteostasis in Health and Disease.Journal of neurochemistry · 2026
    Review
  2. Review
  3. Article
  4. Robust mammalian RNA localization elements are complex and multipartite.bioRxiv : the preprint server for biology · 2026
    Article
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  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Mitochondrial Dysfunction in Spinal Muscular Atrophy.International journal of molecular sciences · 2022
    Review
  18. Article
  19. Transcriptome-scale methods for uncovering subcellular RNA localization mechanisms.Biochimica et biophysica acta. Molecular cell research · 2022
    Review
  20. Review

6 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Lena SaalInstitute for Clinical Neurobiology, University of Wuerzburg, D 97078 Wuerzburg, Germany.
Michael BrieseInstitute for Clinical Neurobiology, University of Wuerzburg, D 97078 Wuerzburg, Germany.
Susanne KneitzDepartment of Physiological Chemistry I, Biocenter, University of Wuerzburg, D 97074 Wuerzburg, Germany.
Michael GlinkaInstitute for Clinical Neurobiology, University of Wuerzburg, D 97078 Wuerzburg, Germany.
Michael SendtnerInstitute for Clinical Neurobiology, University of Wuerzburg, D 97078 Wuerzburg, Germany Sendtner_M@ukw.de.
University of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal function critically depends on coordinated subcellular distribution of mRNAs. Disturbed mRNA processing and axonal transport has been found in spinal muscular atrophy and could be causative for dysfunction and degeneration of motoneurons. Despite the advances made in characterizing the transport mechanisms of several axonal mRNAs, an unbiased approach to identify the axonal repertoire of mRNAs in healthy and degenerating motoneurons has been lacking. Here we used compartmentalized microfluidic chambers to investigate the somatodendritic and axonal mRNA content of cultured motoneurons by microarray analysis. In axons, transcripts related to protein synthesis and energy production were enriched relative to the somatodendritic compartment. Knockdown of Smn, the protein deficient in spinal muscular atrophy, produced a large number of transcript alterations in both compartments. Transcripts related to immune functions, including MHC class I genes, and with roles in RNA splicing were up-regulated in the somatodendritic compartment. On the axonal side, transcripts associated with axon growth and synaptic activity were down-regulated. These alterations provide evidence that subcellular localization of transcripts with axonal functions as well as regulation of specific transcripts with nonautonomous functions is disturbed in Smn-deficient motoneurons, most likely contributing to the pathophysiology of spinal muscular atrophy.

Indexed as

AnimalsAxonsCell Culture TechniquesCell DifferentiationCells, CulturedEmbryo, MammalianGene Expression RegulationGene Knockdown TechniquesHEK293 CellsHumansMiceMolecular Sequence DataMotor NeuronsMuscular Atrophy, SpinalOligonucleotide Array Sequence AnalysisSurvival of Motor Neuron 1 ProteinSmn1 protein, mouseSurvival of Motor Neuron 1 Proteinaxoncompartmentmotoneuronspinal muscular atrophy

Identifiers

PMID25246652
PMCPMC4201830
OpenAlexW2108531896

What OpenQuestion holds

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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.