Evidence map›Paper›PMID 26672765›Full record

ArticleOncotarget2016

Genome-wide identification of Wig-1 mRNA targets by RIP-Seq analysis.

Cinzia Bersani, Mikael Huss, Stefania Giacomello, Li-Di Xu, Julie Bianchi, Sofi Eriksson, Fredrik Jerhammar, Andrey Alexeyenko, Anna Vilborg, Joakim Lundeberg and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  5. Review
  6. Review
  7. Zmat3 splices together p53-dependent tumor suppression.Molecular & cellular oncology · 2021
    Article
  8. Article
  9. Article
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  11. Evolutionary bioinformatics online · 2020
    Article
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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 4 institutions in 2 countries.

Cinzia BersaniDepartment of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska, Stockholm, Sweden.
Mikael HussScience for Life Laboratory, School of Biotechnology, Royal Institute of Technology, Solna, Sweden.
Stefania GiacomelloScience for Life Laboratory, School of Biotechnology, Royal Institute of Technology, Solna, Sweden.
Li-Di XuDepartment of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska, Stockholm, Sweden.
Julie BianchiDepartment of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska, Stockholm, Sweden.
Sofi ErikssonDepartment of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska, Stockholm, Sweden.
Fredrik JerhammarDepartment of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska, Stockholm, Sweden.
Andrey AlexeyenkoDepartment of Microbiology, Tumour and Cell biology, Bioinformatics Infrastructure for Life Sciences, Science for Life Laboratory, Karolinska Institutet, Stockholm, Sweden.
Anna VilborgDepartment of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT, USA.
Joakim LundebergScience for Life Laboratory, School of Biotechnology, Royal Institute of Technology, Solna, Sweden.
Weng-Onn LuiDepartment of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska, Stockholm, Sweden.
Klas G WimanDepartment of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska, Stockholm, Sweden.
Karolinska Institutet · SEKTH Royal Institute of Technology · SEScience for Life Laboratory · SEYale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RNA-binding proteins (RBPs) play important roles in the regulation of gene expression through a variety of post-transcriptional mechanisms. The p53-induced RBP Wig-1 (Zmat3) binds RNA through its zinc finger domains and enhances stability of p53 and N-Myc mRNAs and decreases stability of FAS mRNA. To identify novel Wig-1-bound RNAs, we performed RNA-immunoprecipitation followed by high-throughput sequencing (RIP-Seq) in HCT116 and Saos-2 cells. We identified 286 Wig-1-bound mRNAs common between the two cell lines. Sequence analysis revealed that AU-rich elements (AREs) are highly enriched in the 3'UTR of these Wig-1-bound mRNAs. Network enrichment analysis showed that Wig-1 preferentially binds mRNAs involved in cell cycle regulation. Moreover, we identified a 2D Wig-1 binding motif in HIF1A mRNA. Our findings confirm that Wig-1 is an ARE-BP that regulates cell cycle-related processes and provide a novel view of how Wig-1 may bind mRNA through a putative structural motif. We also significantly extend the repertoire of Wig-1 target mRNAs. Since Wig-1 is a transcriptional target of the tumor suppressor p53, these results have implications for our understanding of p53-dependent stress responses and tumor suppression.

Indexed as

TranscriptomeBlotting, WesternBone NeoplasmsCarrier ProteinsGene OntologyGene Regulatory NetworksHCT116 CellsHigh-Throughput Nucleotide SequencingHumansImmunoprecipitationNuclear ProteinsOsteosarcomaReal-Time Polymerase Chain ReactionResponse ElementsReverse Transcriptase Polymerase Chain ReactionRNA-Binding ProteinsCarrier ProteinsNuclear ProteinsRNA-Binding ProteinsRNA, MessengerTP53 protein, humanTumor Suppressor Protein p53ZMAT3 protein, humanAREscell cyclep53RIP-SeqWig-1

Identifiers

PMID26672765
PMCPMC4811505
OpenAlexW2217732376

What OpenQuestion holds

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LicenceCC BY
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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.