Evidence map›Paper›PMID 27651463›Full record

ArticleNucleic acids research2017

The dual role of LSD1 and HDAC3 in STAT5-dependent transcription is determined by protein interactions, binding affinities, motifs and genomic positions.

Aikaterini Nanou, Chrisavgi Toumpeki, Matthieu D Lavigne, Vassiliki Lazou, Jeroen Demmers, Triantafillos Paparountas, Dimitris Thanos, Eleni Katsantoni

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

18 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. JAK-STAT in Early Hematopoiesis and Leukemia.Frontiers in cell and developmental biology · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Recent Update of HDAC Inhibitors in Lymphoma.Frontiers in cell and developmental biology · 2020
    Review
  15. Review
  16. Article
  17. Article
  18. 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.

Aikaterini NanouBasic Research Center, Biomedical Research Foundation, Academy of Athens, Soranou tou Ephessiou 4, 115 27 Athens, Greece.
Chrisavgi ToumpekiBasic Research Center, Biomedical Research Foundation, Academy of Athens, Soranou tou Ephessiou 4, 115 27 Athens, Greece.
Matthieu D LavigneBasic Research Center, Biomedical Research Foundation, Academy of Athens, Soranou tou Ephessiou 4, 115 27 Athens, Greece.
Vassiliki LazouBasic Research Center, Biomedical Research Foundation, Academy of Athens, Soranou tou Ephessiou 4, 115 27 Athens, Greece.
Jeroen DemmersProteomics Center, Erasmus Medical Center, Wytemaweg 80, 3015 CN Rotterdam, The Netherlands.
Triantafillos PaparountasBasic Research Center, Biomedical Research Foundation, Academy of Athens, Soranou tou Ephessiou 4, 115 27 Athens, Greece.
Dimitris ThanosBasic Research Center, Biomedical Research Foundation, Academy of Athens, Soranou tou Ephessiou 4, 115 27 Athens, Greece.
Eleni KatsantoniBasic Research Center, Biomedical Research Foundation, Academy of Athens, Soranou tou Ephessiou 4, 115 27 Athens, Greece ekatsantoni@bioacademy.gr.
Academy of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

STAT5 interacts with other factors to control transcription, and the mechanism of regulation is of interest as constitutive active STAT5 has been reported in malignancies. Here, LSD1 and HDAC3 were identified as novel STAT5a interacting partners in pro-B cells. Characterization of STAT5a, LSD1 and HDAC3 target genes by ChIP-seq and RNA-seq revealed gene subsets regulated by independent or combined action of the factors and LSD1/HDAC3 to play dual role in their activation or repression. Genes bound by STAT5a alone or in combination with weakly associated LSD1 or HDAC3 were enriched for the canonical STAT5a GAS motif, and such binding induced activation or repression. Strong STAT5 binding was seen more frequently in intergenic regions, which might function as distal enhancer elements. Groups of genes bound weaker by STAT5a and stronger by LSD1/HDAC3 showed an absence of the GAS motif, and were differentially regulated based on their genomic binding localization and binding affinities. These genes exhibited increased binding frequency in promoters, and in conjunction with the absence of GAS sites, the data indicate a requirement for stabilization by additional factors, which might recruit LSD1/HDAC3. Our study describes an interaction network of STAT5a/LSD1/HDAC3 and a dual function of LSD1/HDAC3 on STAT5-dependent transcription, defined by protein-protein interactions, genomic binding localization/affinity and motifs.

Indexed as

Transcription, GeneticAnimalsBinding SitesB-LymphocytesCell Line, TumorCloning, MolecularEscherichia coliGene Expression RegulationHigh-Throughput Nucleotide SequencingHistone Deacetylase 3Histone DeacetylasesHistone DemethylasesMiceNucleotide MotifsPromoter Regions, GeneticProtein BindingHistone Deacetylase 3Histone DeacetylasesHistone DemethylasesKDM1a protein, mouseRecombinant Fusion ProteinsStat5a protein, mouseSTAT5 Transcription Factor

Identifiers

PMID27651463
PMCPMC5224505
OpenAlexW2522255269

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.