Evidence map›Paper›PMID 17311813›Full record

ArticleNucleic acids research2007

Ovol1 represses its own transcription by competing with transcription activator c-Myb and by recruiting histone deacetylase activity.

Mahalakshmi Nair, Virginia Bilanchone, Kori Ortt, Satrajit Sinha, Xing Dai

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. OVO-like 1 regulates progenitor cell fate in human trophoblast development.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  12. Article
  13. Article
  14. Review
  15. Genetic risk factors for the development of allergic disease identified by genome-wide association.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2015
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

5 authors at 2 institutions in 1 country.

Mahalakshmi NairDepartment of Biological Chemistry, School of Medicine, Developmental Biology Center, University of California, Irvine, CA 92697, USA.
Virginia Bilanchone
Kori Ortt
Satrajit Sinha
Xing Dai
University at Buffalo, State University of New York · USUniversity of California, Irvine · US

Funding

Role of Ovol Genes in Epidermal DevelopmentR01AR047320 · NIAMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI DAI, XING · 2001 to 2010
$3.2M
Movo in embryonic development and skin differentiationK02AR051482 · NIAMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI DAI, XING · 2004 to 2008
$405k
NIAMS NIH HHS K02 AR051482NIAMS NIH HHS K02-AR51482NIAMS NIH HHS R01 AR047320NIAMS NIH HHS R01-AR47320
6 · The paper itself

Abstract

Ovol1 belongs to a family of evolutionarily conserved zinc finger proteins that act downstream of key developmental signaling pathways such as Wnt and TGF-beta/BMP. It plays important roles in epithelial and germ cell development, particularly by repressing c-Myc and Id2 genes and modulating the balance between proliferation and differentiation of progenitor cells. In this study, we show that Ovol1 negatively regulates its own expression by binding to and repressing the activity of its promoter. We further demonstrate that Ovol1 uses both passive and active repression mechanisms to auto-repress: (1) it antagonizes transcriptional activation of c-Myb, a known positive regulator of proliferation, by competing for DNA binding; (2) it recruits histone deacetylase activity to the promoter via an N-terminal SNAG repressor domain. At Ovol1 cognate sites in the endogenous Ovol1 promoter, c-Myb binding correlates with increased histone acetylation, whereas the expression of Ovol1 correlates with a displacement of c-Myb from the DNA and decreased histone acetylation. Collectively, our data suggest that Ovol1 restricts its own expression by counteracting c-Myb activation and histone acetylation of the Ovol1 promoter.

Indexed as

Gene Expression RegulationAcetylationAnimalsBinding, CompetitiveBinding SitesCell LineDNA-Binding ProteinsHistone DeacetylasesHistonesMicePromoter Regions, GeneticProtein Structure, TertiaryProto-Oncogene Proteins c-mybRepressor ProteinsTrans-ActivatorsTranscription FactorsDNA-Binding ProteinsHistone DeacetylasesHistonesOvo1 protein, mouseProto-Oncogene Proteins c-mybRepressor ProteinsTrans-ActivatorsTranscription Factors

Identifiers

PMID17311813
PMCPMC1865076
OpenAlexW2011615793

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.