Evidence map›Paper›PMID 30388410›Full record

ArticleMolecular cell2018

Exon Junction Complexes Suppress Spurious Splice Sites to Safeguard Transcriptome Integrity.

Volker Boehm, Thiago Britto-Borges, Anna-Lena Steckelberg, Kusum K Singh, Jennifer V Gerbracht, Elif Gueney, Lorea Blazquez, Janine Altmüller, Christoph Dieterich, Niels H Gehring

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Article in Molecular cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing 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

52 citing papers in PubMed.

  1. Article
  2. TAR syndrome causal genebioRxiv : the preprint server for biology · 2026
    Article
  3. Detection of a sequence feature for recursive splicing.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Gene regulation through exon junction complex modularity.Nature structural & molecular biology · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Volker BoehmInstitute for Genetics, University of Cologne, 50674 Cologne, Germany.
Thiago Britto-BorgesSection of Bioinformatics and Systems Cardiology, Department of Internal Medicine III and Klaus Tschira Institute for Integrative Computational Cardiology, University of Heidelberg, 69120 Heidelberg, Germany; DZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, 69120 Heidelberg, Germany.
Anna-Lena SteckelbergInstitute for Genetics, University of Cologne, 50674 Cologne, Germany; Department of Biochemistry and Molecular Genetics, University of Colorado Denver School of Medicine, Aurora, CO 80045, USA.
Kusum K SinghInstitute for Genetics, University of Cologne, 50674 Cologne, Germany; Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati, 781039-Guwahati, Assam, India.
Jennifer V GerbrachtInstitute for Genetics, University of Cologne, 50674 Cologne, Germany.
Elif GueneyInstitute for Genetics, University of Cologne, 50674 Cologne, Germany.
Lorea BlazquezDepartment of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London WC1N 3BG, UK; The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Janine AltmüllerCologne Center for Genomics (CCG), University of Cologne, 50931 Cologne, Germany; Institute of Human Genetics, University of Cologne, 50931 Cologne, Germany; Center for Molecular Medicine Cologne, University of Cologne, 50937 Cologne, Germany.
Christoph DieterichSection of Bioinformatics and Systems Cardiology, Department of Internal Medicine III and Klaus Tschira Institute for Integrative Computational Cardiology, University of Heidelberg, 69120 Heidelberg, Germany; DZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, 69120 Heidelberg, Germany. Electronic address: christoph.dieterich@uni-heidelberg.de.
Niels H GehringInstitute for Genetics, University of Cologne, 50674 Cologne, Germany. Electronic address: ngehring@uni-koeln.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Productive splicing of human precursor messenger RNAs (pre-mRNAs) requires the correct selection of authentic splice sites (SS) from the large pool of potential SS. Although SS consensus sequence and splicing regulatory proteins are known to influence SS usage, the mechanisms ensuring the effective suppression of cryptic SS are insufficiently explored. Here, we find that many aberrant exonic SS are efficiently silenced by the exon junction complex (EJC), a multi-protein complex that is deposited on spliced mRNA near the exon-exon junction. Upon depletion of EJC proteins, cryptic SS are de-repressed, leading to the mis-splicing of a broad set of mRNAs. Mechanistically, the EJC-mediated recruitment of the splicing regulator RNPS1 inhibits cryptic 5'SS usage, while the deposition of the EJC core directly masks reconstituted 3'SS, thereby precluding transcript disintegration. Thus, the EJC protects the transcriptome of mammalian cells from inadvertent loss of exonic sequences and safeguards the expression of intact, full-length mRNAs.

Indexed as

Alternative SplicingConsensus SequenceDEAD-box RNA HelicasesEukaryotic Initiation Factor-4AExonsHeLa CellsHumansIntronsRibonucleoproteinsRNA-Binding ProteinsRNA, MessengerRNA PrecursorsRNA Splice SitesRNA SplicingTranscriptomeDEAD-box RNA HelicasesEIF4A3 protein, humanEukaryotic Initiation Factor-4ARBM8A protein, humanRibonucleoproteinsRNA-Binding ProteinsRNA, MessengerRNA PrecursorsRNA Splice SitesRNPS1 protein, humanalternative splicingcryptic splice sitesEJCexon junction complexgene expressionmRNA processing

Identifiers

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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.