Evidence map›Paper›PMID 21454521›Full record

ArticleThe Journal of biological chemistry2011

The developmental regulator protein Gon4l associates with protein YY1, co-repressor Sin3a, and histone deacetylase 1 and mediates transcriptional repression.

Ping Lu, Isaiah L Hankel, Bruce S Hostager, Julie A Swartzendruber, Ann D Friedman, Janet L Brenton, Paul B Rothman, John D Colgan

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Article
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  9. FGFR2 genetic variants in women with breast cancer.Molecular medicine reports · 2023
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  10. Review
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  13. Article
  14. Article
  15. Article
  16. Article
  17. YY1 promotes colorectal cancer proliferation through theAmerican journal of cancer research · 2019
    Article
  18. Article
  19. Article
  20. 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

8 authors at 2 institutions in 2 countries.

Ping LuInterdisciplinary Immunology Graduate Program, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA.
Isaiah L Hankel
Bruce S Hostager
Julie A Swartzendruber
Ann D Friedman
Janet L Brenton
Paul B Rothman
John D Colgan
University of Iowa · USInstitute of Immunology · HR

Funding

Regulation of Atopic Immune Responses by the Prolyl lsomerase Cyclophillin AR01AI067489 · NIAID · UNIVERSITY OF IOWA · PI COLGAN, JOHN D · 2006 to 2010
$1.8M
NIAID NIH HHS R01 AI067489NIAID NIH HHS R01AI067489
6 · The paper itself

Abstract

Genetic studies involving zebrafish and mice have demonstrated that the protein Gon4l (Gon4-like) is essential for hematopoiesis. These studies also suggested that Gon4l regulates gene expression during hematopoietic development, yet the biochemical function of Gon4l has not been defined. Here, we describe the identification of factors that interact with Gon4l and may cooperate with this protein to regulate gene expression. As predicted by polypeptide sequence conservation, Gon4l interacted and co-localized with the DNA-binding protein YY1 (Yin Yang 1). Density gradient sedimentation analysis of protein lysates from mouse M12 B cells showed that Gon4l and YY1 co-sediment with the transcriptional co-repressor Sin3a and its functional partner histone deacetylase (HDAC) 1. Consistent with these results, immunoprecipitation studies showed that Gon4l associates with Sin3a, HDAC1, and YY1 as a part of complexes that form in M12 cells. Sequential immunoprecipitation studies demonstrated that Gon4l, YY1, Sin3a, and HDAC1 could all associate as components of a single complex and that a conserved domain spanning the central portion of Gon4l was required for formation of this complex. When targeted to DNA, Gon4l repressed the activity of a nearby promoter, which correlated with the ability to interact with Sin3a and HDAC1. Our data suggest that Sin3a, HDAC1, and YY1 are co-factors for Gon4l and that Gon4l may function as a platform for the assembly of complexes that regulate gene expression.

Indexed as

AnimalsCo-Repressor ProteinsDNA-Binding ProteinsDrosophila melanogasterGene Expression RegulationHEK293 CellsHistone Deacetylase 1HumansMiceMultiprotein ComplexesRepressor ProteinsSin3 Histone Deacetylase and Corepressor ComplexTranscription FactorsTranscription, GeneticYY1 Transcription FactorZebrafishCo-Repressor ProteinsDNA-Binding ProteinsGON4L protein, humanHDAC1 protein, humanHistone Deacetylase 1Multiprotein ComplexesRepressor ProteinsSIN3A transcription factorSin3 Histone Deacetylase and Corepressor ComplexTranscription FactorsYY1 protein, humanYY1 Transcription Factor

Identifiers

PMID21454521
PMCPMC3093903
OpenAlexW2048359567

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.