Evidence map›Paper›PMID 31732746›Full record

ArticleNucleic acids research2019

The mRNA repressor TRIM71 cooperates with Nonsense-Mediated Decay factors to destabilize the mRNA of CDKN1A/p21.

Lucia A Torres-Fernández, Bettina Jux, Maximilian Bille, Yasmine Port, Karin Schneider, Matthias Geyer, Günter Mayer, Waldemar Kolanus

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

33 citing papers in PubMed, 46 citations in OpenAlex.

  1. Trial
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  12. Tripartite motif 2b (Journal of virology · 2024
    Article
  13. Article
  14. Review
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  16. Article
  17. A neural stem cell paradigm of pediatric hydrocephalus.Cerebral cortex (New York, N.Y. : 1991) · 2023
    Article
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  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

8 authors at 1 institution in 1 country.

Lucia A Torres-FernándezMolecular Immunology and Cell Biology, Life & Medical Sciences Institute (LIMES), University of Bonn, 53115 Bonn, Germany.
Bettina JuxMolecular Immunology and Cell Biology, Life & Medical Sciences Institute (LIMES), University of Bonn, 53115 Bonn, Germany.
Maximilian BilleMolecular Immunology and Cell Biology, Life & Medical Sciences Institute (LIMES), University of Bonn, 53115 Bonn, Germany.
Yasmine PortMolecular Immunology and Cell Biology, Life & Medical Sciences Institute (LIMES), University of Bonn, 53115 Bonn, Germany.
Karin SchneiderMolecular Immunology and Cell Biology, Life & Medical Sciences Institute (LIMES), University of Bonn, 53115 Bonn, Germany.
Matthias GeyerInstitute of Structural Biology, University Clinics Bonn, University of Bonn, 53127 Bonn, Germany.
Günter MayerCenter of Aptamer Research & Development; Chemical Biology & Chemical Genetics, Life & Medical Sciences Institute (LIMES). University of Bonn, 53121 Bonn, Germany.
Waldemar KolanusMolecular Immunology and Cell Biology, Life & Medical Sciences Institute (LIMES), University of Bonn, 53115 Bonn, Germany.
University of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonsense-mediated decay (NMD) plays a fundamental role in the degradation of premature termination codon (PTC)-containing transcripts, but also regulates the expression of functional transcripts lacking PTCs, although such 'non-canonical' functions remain ill-defined and require the identification of factors targeting specific mRNAs to the NMD machinery. Our work identifies the stem cell-specific mRNA repressor protein TRIM71 as one of these factors. TRIM71 plays an essential role in embryonic development and is linked to carcinogenesis. For instance, TRIM71 has been correlated with advanced stages and poor prognosis in hepatocellular carcinoma. Our data shows that TRIM71 represses the mRNA of the cell cycle inhibitor and tumor suppressor CDKN1A/p21 and promotes the proliferation of HepG2 tumor cells. CDKN1A specific recognition involves the direct interaction of TRIM71 NHL domain with a structural RNA stem-loop motif within the CDKN1A 3'UTR. Importantly, CDKN1A repression occurs independently of miRNA-mediated silencing. Instead, the NMD factors SMG1, UPF1 and SMG7 assist TRIM71-mediated degradation of CDKN1A mRNA, among other targets. Our data sheds light on TRIM71-mediated target recognition and repression mechanisms and uncovers a role for this stem cell-specific factor and oncogene in non-canonical NMD, revealing the existence of a novel mRNA surveillance mechanism which we have termed the TRIM71/NMD axis.

Indexed as

RNA Stability3' Untranslated RegionsCyclin-Dependent Kinase Inhibitor p21HEK293 CellsHep G2 CellsHumansNonsense Mediated mRNA DecayProtein BindingRepressor ProteinsRNA, MessengerTripartite Motif ProteinsUbiquitin-Protein Ligases3' Untranslated RegionsCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Repressor ProteinsRNA, MessengerTRIM71 protein, humanTripartite Motif ProteinsUbiquitin-Protein Ligases

Identifiers

PMID31732746
PMCPMC7145526
OpenAlexW2986220076

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.