Evidence map›Paper›PMID 26656492›Full record

ArticleNucleic acids research2016

A novel role for CARM1 in promoting nonsense-mediated mRNA decay: potential implications for spinal muscular atrophy.

Gabriel Sanchez, Emma Bondy-Chorney, Janik Laframboise, Geneviève Paris, Andréanne Didillon, Bernard J Jasmin, Jocelyn Côté

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-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

21 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Carm1 and the Epigenetic Control of Stem Cell Function.Stem cells translational medicine · 2022
    Article
  9. Review
  10. Review
  11. Article
  12. PRMT4 drives post-ischemic angiogenesis via YB1/VEGF signaling.Journal of molecular medicine (Berlin, Germany) · 2021
    Article
  13. Review
  14. Blocking the Spinal Fbxo3/CARM1/KNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Article
  15. Review
  16. CARM1 suppressesThe Journal of biological chemistry · 2018
    Article
  17. Review
  18. Review
  19. Diverse role of survival motor neuron protein.Biochimica et biophysica acta. Gene regulatory mechanisms · 2017
    Review
  20. 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

7 authors at 1 institution in 1 country.

Gabriel SanchezCentre for Neuromuscular Disease, Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.
Emma Bondy-ChorneyCentre for Neuromuscular Disease, Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.
Janik LaframboiseCentre for Neuromuscular Disease, Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.
Geneviève ParisCentre for Neuromuscular Disease, Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.
Andréanne DidillonCentre for Neuromuscular Disease, Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.
Bernard J JasminCentre for Neuromuscular Disease, Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.
Jocelyn CôtéCentre for Neuromuscular Disease, Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada jcote@uottawa.ca.
University of Ottawa · CA

Funding

Canadian Institutes of Health Research MOP-86746
6 · The paper itself

Abstract

Loss of 'Survival of Motor Neurons' (SMN) leads to spinal muscular atrophy (SMA), a disease characterized by degeneration of spinal cord alpha motor neurons, resulting in muscle weakness, paralysis and death during early childhood. SMN is required for assembly of the core splicing machinery, and splicing defects were documented in SMA. We previously uncovered that Coactivator-Associated Methyltransferase-1 (CARM1) is abnormally up-regulated in SMA, leading to mis-regulation of a number of transcriptional and alternative splicing events. We report here that CARM1 can promote decay of a premature terminating codon (PTC)-containing mRNA reporter, suggesting it can act as a mediator of nonsense-mediated mRNA decay (NMD). Interestingly, this pathway, while originally perceived as solely a surveillance mechanism preventing expression of potentially detrimental proteins, is now emerging as a highly regulated RNA decay pathway also acting on a subset of normal mRNAs. We further show that CARM1 associates with major NMD factor UPF1 and promotes its occupancy on PTC-containing transcripts. Finally, we identify a specific subset of NMD targets that are dependent on CARM1 for degradation and that are also misregulated in SMA, potentially adding exacerbated targeting of PTC-containing mRNAs to the already complex array of molecular defects associated with this disease.

Indexed as

Nonsense Mediated mRNA DecayAlternative SplicingAnimalsCell LineCodon, TerminatorExonsHumansIntronsMiceMice, Inbred C57BLMotor NeuronsMuscular Atrophy, SpinalProtein-Arginine N-MethyltransferasesRNA HelicasesRNA, MessengerSpinal Cordcoactivator-associated arginine methyltransferase 1Codon, TerminatorProtein-Arginine N-MethyltransferasesRNA HelicasesRNA, MessengerTrans-ActivatorsUPF1 protein, human

Identifiers

PMID26656492
PMCPMC4824080
OpenAlexW2289696946

What OpenQuestion holds

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Read underepoch 390

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.