Evidence map›Paper›PMID 16782888›Full record

ArticleMolecular and cellular biology2006

Btg2 enhances retinoic acid-induced differentiation by modulating histone H4 methylation and acetylation.

Daniela Passeri, Antonella Marcucci, Giovanni Rizzo, Monia Billi, Maddalena Panigada, Luca Leonardi, Felice Tirone, Francesco Grignani

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

37 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Article
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  4. International journal of molecular sciences · 2023
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  5. The Cxcr2Frontiers in immunology · 2023
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  6. Review
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  8. International journal of general medicine · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Tumor suppressors BTG1 and BTG2: Beyond growth control.Journal of cellular physiology · 2019
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

8 authors at 2 institutions in 1 country.

Daniela PasseriPatologia Generale and Medicina Interna e Scienze Oncologiche, Dipartimento di Medicina Clinica e Sperimentale, Perugia University, Policlinico Monteluce, Perugia, Italy.
Antonella Marcucci
Giovanni Rizzo
Monia Billi
Maddalena Panigada
Luca Leonardi
Felice Tirone
Francesco Grignani
University of Perugia · ITInstitute of Neurobiology and Molecular Medicine · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinoic acid controls hematopoietic differentiation through the transcription factor activity of its receptors. They act on specific target genes by recruiting protein complexes that deacetylate or acetylate histones and modify chromatin status. The regulation of this process is affected by histone methyltransferases, which can inhibit or activate transcription depending on their amino acid target. We show here that retinoic acid treatment of hematopoietic cells induces the expression of BTG2. Overexpression of this protein increases RARalpha transcriptional activity and the differentiation response to retinoic acid of myeloid leukemia cells and CD34+ hematopoietic progenitors. In the absence of retinoic acid, BTG2 is present in the RARalpha transcriptional complex, together with the arginine methyltransferase PRMT1 and Sin3A. Overexpressed BTG2 increases PRMT1 participation in the RARalpha protein complex on the RARbeta promoter, a target gene model, and enhances gene-specific histone H4 arginine methylation. Upon RA treatment Sin3A, BTG2, and PRMT1 detach from RARalpha and thereafter BGT2 and PRMT1 are driven to the cytoplasm. These events prime histone H4 demethylation and acetylation. Overall, our data show that BTG2 contributes to retinoic acid activity by favoring differentiation through a gene-specific modification of histone H4 arginine methylation and acetylation levels.

Indexed as

Gene Expression RegulationAcetylationArginineCell DifferentiationCell Line, TumorGenes, Tumor SuppressorHematopoietic Stem CellsHistonesHumansImmediate-Early ProteinsMethylationPromoter Regions, GeneticProtein-Arginine N-MethyltransferasesReceptors, Retinoic AcidRepressor ProteinsRetinoic Acid Receptor alphaArginineBTG2 protein, humanHistonesImmediate-Early ProteinsPRMT1 protein, humanProtein-Arginine N-MethyltransferasesRARA protein, humanReceptors, Retinoic AcidRepressor ProteinsRetinoic Acid Receptor alphaSIN3A transcription factorSin3 Histone Deacetylase and Corepressor ComplexTretinoinTumor Suppressor Proteins

Identifiers

PMID16782888
PMCPMC1489145
OpenAlexW2051508016

What OpenQuestion holds

Textmetadata
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.