Evidence map›Paper›PMID 25692239›Full record

ArticleRNA biology2014

Splicing changes in SMA mouse motoneurons and SMN-depleted neuroblastoma cells: evidence for involvement of splicing regulatory proteins.

Qing Huo, Melis Kayikci, Philipp Odermatt, Kathrin Meyer, Olivia Michels, Smita Saxena, Jernej Ule, Daniel Schümperli

Open access · bronzeAbstract read
In one paragraph

Article in RNA biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Mitochondrial Dysfunction in Spinal Muscular Atrophy.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Review
  9. Review
  10. Hyperexcitability precedes motoneuron loss in theJournal of neurophysiology · 2019
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Somatic Therapy of a Mouse SMA Model with a U7 snRNA Gene Correcting SMN2 Splicing.Molecular therapy : the journal of the American Society of Gene Therapy · 2016
    Article
  19. Article
  20. 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

8 authors at 2 institutions in 5 countries.

Qing Huoa Institute of Cell Biology ; University of Bern ; Bern , Switzerland.
Melis Kayikci
Philipp Odermatt
Kathrin Meyer
Olivia Michels
Smita Saxena
Jernej Ule
Daniel Schümperli
University of Bern · CHMRC Laboratory of Molecular Biology · GB

Funding

Medical Research Council MC_U105185858
6 · The paper itself

Abstract

Spinal Muscular Atrophy (SMA) is caused by deletions or mutations in the Survival Motor Neuron 1 (SMN1) gene. The second gene copy, SMN2, produces some, but not enough, functional SMN protein. SMN is essential to assemble small nuclear ribonucleoproteins (snRNPs) that form the spliceosome. However, it is not clear whether SMA is caused by defects in this function that could lead to splicing changes in all tissues, or by the impairment of an additional, less well characterized, but motoneuron-specific SMN function. We addressed the first possibility by exon junction microarray analysis of motoneurons (MNs) isolated by laser capture microdissection from a severe SMA mouse model. This revealed changes in multiple U2-dependent splicing events. Moreover, splicing appeared to be more strongly affected in MNs than in other cells. By testing mutiple genes in a model of progressive SMN depletion in NB2a neuroblastoma cells, we obtained evidence that U2-dependent splicing changes occur earlier than U12-dependent ones. As several of these changes affect genes coding for splicing regulators, this may acerbate the splicing response induced by low SMN levels and induce secondary waves of splicing alterations.

Indexed as

Gene Expression RegulationRNA SplicingAnimalsBlotting, WesternCell Line, TumorCells, CulturedHumansIntronsMembrane ProteinsMiceMice, KnockoutMice, TransgenicMotor NeuronsMuscular Atrophy, SpinalNeuroblastomaReverse Transcriptase Polymerase Chain ReactionMembrane ProteinsRbfox1 protein, mouseRNA-Binding ProteinsRNA Splicing Factorsseptin 9, mouseSeptinsSMN Complex ProteinsTmem41b protein, mouseESE, exonic splicing enhancerexon junction microarrayFCS, fetal calf serumhz, heterozygote, LCMlaser capture microdissectionmajor spliceosomeminor spliceosomeMN, motoneuronmotoneuronsneurodegerative diseaseNMD, nonsense-mediated mRNA decayNMJ, neuromuscular junction, PCRpolymerase chain reaction, qPCRreal-time (quantitative) PCRRT, reverse transcriptionsh, short hairpinSMA, Spinal Muscular AtrophySMN, Survival Motor NeuronsnRNA, small nuclear ribonucleic acidsnRNP assemblysnRNP, small nuclear ribonucleoproteinSpinal Muscular Atrophysplicingsplicing regulatorsTcRβ, T-cell receptor β chain

Identifiers

PMID25692239
PMCPMC4601534
OpenAlexW1512545662

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.