Evidence map›Paper›PMID 21949697›Full record

ArticlePloS one2011

Characterisation of genome-wide PLZF/RARA target genes.

Salvatore Spicuglia, Christelle Vincent-Fabert, Touati Benoukraf, Guillaume Tibéri, Andrew J Saurin, Joaquin Zacarias-Cabeza, David Grimwade, Ken Mills, Boris Calmels, François Bertucci and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. miR-183-5p Inhibits Occurrence and Progression of Acute Myeloid Leukemia via Targeting Erbin.Molecular therapy : the journal of the American Society of Gene Therapy · 2019
    Article
  4. Article
  5. Molecular Heterogeneity in Acute Promyelocytic Leukemia - a Single Center Experience from India.Mediterranean journal of hematology and infectious diseases · 2018
    Article
  6. Eya2, a Target Activated by Plzf, Is Critical forMolecular and cellular biology · 2017
    Article
  7. Article
  8. Review
  9. Article
  10. RARα-PLZF oncogene inhibits C/EBPα function in myeloid cells.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  11. Article
  12. Article
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

13 authors at 7 institutions in 3 countries.

Salvatore SpicugliaCentre d'Immunologie de Marseille-Luminy, Université de la Méditerranée, Campus de Luminy, Marseille, France.
Christelle Vincent-Fabert
Touati Benoukraf
Guillaume Tibéri
Andrew J Saurin
Joaquin Zacarias-Cabeza
David Grimwade
Ken Mills
Boris Calmels
François Bertucci
Michael Sieweke
Pierre Ferrier
Estelle Duprez
Inserm · FRCentre National de la Recherche Scientifique · FRCentre de Recherche en Cancérologie de Marseille · FRCentre d’Immunologie de Marseille-Luminy · FRKing's College London · GBNational University of Singapore · SGQueen's University Belfast · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The PLZF/RARA fusion protein generated by the t(11;17)(q23;q21) translocation in acute promyelocytic leukaemia (APL) is believed to act as an oncogenic transcriptional regulator recruiting epigenetic factors to genes important for its transforming potential. However, molecular mechanisms associated with PLZF/RARA-dependent leukaemogenesis still remain unclear.We searched for specific PLZF/RARA target genes by ChIP-on-chip in the haematopoietic cell line U937 conditionally expressing PLZF/RARA. By comparing bound regions found in U937 cells expressing endogenous PLZF with PLZF/RARA-induced U937 cells, we isolated specific PLZF/RARA target gene promoters. We next analysed gene expression profiles of our identified target genes in PLZF/RARA APL patients and analysed DNA sequences and epigenetic modification at PLZF/RARA binding sites. We identify 413 specific PLZF/RARA target genes including a number encoding transcription factors involved in the regulation of haematopoiesis. Among these genes, 22 were significantly down regulated in primary PLZF/RARA APL cells. In addition, repressed PLZF/RARA target genes were associated with increased levels of H3K27me3 and decreased levels of H3K9K14ac. Finally, sequence analysis of PLZF/RARA bound sequences reveals the presence of both consensus and degenerated RAREs as well as enrichment for tissue-specific transcription factor motifs, highlighting the complexity of targeting fusion protein to chromatin. Our study suggests that PLZF/RARA directly targets genes important for haematopoietic development and supports the notion that PLZF/RARA acts mainly as an epigenetic regulator of its direct target genes.

Indexed as

Gene Expression Regulation, LeukemicGenome-Wide Association StudyAcetylationBinding SitesChromatin ImmunoprecipitationCluster AnalysisGene Expression ProfilingHistonesHumansKruppel-Like Transcription FactorsLeukemia, Promyelocytic, AcuteMethylationOligonucleotide Array Sequence AnalysisOncogene Proteins, FusionPromoter Regions, GeneticPromyelocytic Leukemia Zinc Finger ProteinHistonesKruppel-Like Transcription FactorsOncogene Proteins, FusionPLZF-RARalpha fusion protein, humanPromyelocytic Leukemia Zinc Finger ProteinTranscription FactorsZBTB16 protein, human

Identifiers

PMID21949697
PMCPMC3176768
OpenAlexW2050294631

What OpenQuestion holds

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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.