Evidence map›Paper›PMID 32621609›Full record

ArticleNucleic acids research2020

CASC3 promotes transcriptome-wide activation of nonsense-mediated decay by the exon junction complex.

Jennifer V Gerbracht, Volker Boehm, Thiago Britto-Borges, Sebastian Kallabis, Janica L Wiederstein, Simona Ciriello, Dominik U Aschemeier, Marcus Krüger, Christian K Frese, Janine Altmüller and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 57 citations in OpenAlex.

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  8. Gene regulation through exon junction complex modularity.Nature structural & molecular biology · 2025
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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

12 authors at 2 institutions in 1 country.

Jennifer V GerbrachtInstitute for Genetics, University of Cologne, 50674 Cologne, Germany.
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.
Sebastian KallabisCECAD Research Center, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Janica L WiedersteinCECAD Research Center, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Simona CirielloInstitute for Genetics, University of Cologne, 50674 Cologne, Germany.
Dominik U AschemeierInstitute for Genetics, University of Cologne, 50674 Cologne, Germany.
Marcus KrügerCECAD Research Center, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Christian K FreseCECAD Research Center, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Janine AltmüllerCologne Center for Genomics (CCG), University of Cologne, 50931 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.
Niels H GehringInstitute for Genetics, University of Cologne, 50674 Cologne, Germany.
University of Cologne · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The exon junction complex (EJC) is an essential constituent and regulator of spliced messenger ribonucleoprotein particles (mRNPs) in metazoans. As a core component of the EJC, CASC3 was described to be pivotal for EJC-dependent nuclear and cytoplasmic processes. However, recent evidence suggests that CASC3 functions differently from other EJC core proteins. Here, we have established human CASC3 knockout cell lines to elucidate the cellular role of CASC3. In the knockout cells, overall EJC composition and EJC-dependent splicing are unchanged. A transcriptome-wide analysis reveals that hundreds of mRNA isoforms targeted by nonsense-mediated decay (NMD) are upregulated. Mechanistically, recruiting CASC3 to reporter mRNAs by direct tethering or via binding to the EJC stimulates mRNA decay and endonucleolytic cleavage at the termination codon. Building on existing EJC-NMD models, we propose that CASC3 equips the EJC with the persisting ability to communicate with the NMD machinery in the cytoplasm. Collectively, our results characterize CASC3 as a peripheral EJC protein that tailors the transcriptome by promoting the degradation of EJC-dependent NMD substrates.

Indexed as

Amino Acid SequenceCell NucleusExonsGene Knockout TechniquesHumansNeoplasm ProteinsNonsense Mediated mRNA DecayRibonucleoproteinsRNA-Binding ProteinsRNA, MessengerRNA SplicingTranscriptomeCASC3 protein, humanmessenger ribonucleoproteinNeoplasm ProteinsRibonucleoproteinsRNA-Binding ProteinsRNA, Messenger

Identifiers

PMID32621609
PMCPMC7470949
OpenAlexW3038824336

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LicenceCC BY
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.