Evidence map›Paper›PMID 15060155›Full record

ArticleMolecular and cellular biology2004

Recruitment of N-CoR/SMRT-TBLR1 corepressor complex by unliganded thyroid hormone receptor for gene repression during frog development.

Akihiro Tomita, Daniel R Buchholz, Yun-Bo Shi

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

70 citing papers in PubMed, 115 citations in OpenAlex.

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  19. TBL1Y: a new gene involved in syndromic hearing loss.European journal of human genetics : EJHG · 2019
    Article
  20. Article

10 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Akihiro TomitaSection on Molecular Morphogenesis, Laboratory of Gene Regulation and Development, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-5431, USA.
Daniel R Buchholz
Yun-Bo Shi
Eunice Kennedy Shriver National Institute of Child Health and Human Development · USNational Institutes of Health · US

Funding

Molecular mechanism of thyroid hormone receptor function during metamorphosisZIAHD001901 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI SHI, YUN-BO · 2009 to 2025
$13.1M
Molecular mechanism of thyroid hormone receptor function during metamorphosisZ01HD001901 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI SHI, YUN-BO · 1995 to 2008
$2.1M
6 · The paper itself

Abstract

The corepressors N-CoR (nuclear receptor corepressor) and SMRT (silencing mediator for retinoid and thyroid hormone receptors) interact with unliganded nuclear hormone receptors, including thyroid hormone (T(3)) receptor (TR). Several N-CoR/SMRT complexes containing histone deacetylases have been purified. The best studied among them are N-CoR/SMRT complexes containing TBL1 (transducin beta-like protein 1) or TBLR1 (TBL1-related protein). Despite extensive studies of these complexes, there has been no direct in vivo evidence for the interaction of TBL1 or TBLR1 with TR or the possible involvement of such complexes in gene repression by any nuclear receptors in any animals. Here, we used the frog oocyte system to demonstrate that unliganded TR interacts with TBLR1 and recruits TBLR1 to its chromatinized target promoter in vivo, accompanied by histone deacetylation and gene repression. We further provide evidence to show that the recruitment of TBLR1 or related proteins is important for repression by unliganded TR. To investigate the potential role for TBLR1 complexes during vertebrate development, we made use of T(3)-dependent amphibian metamorphosis as a model. We found that TBLR1, SMRT, and N-CoR are recruited to T(3)-inducible promoters in premetamorphic tadpoles and are released upon T(3) treatment, which induces metamorphosis. More importantly, we demonstrate that the dissociation of N-CoR/SMRT-TBLR1 complexes from endogenous TR target promoters is correlated with the activation of these genes during spontaneous metamorphosis. Taken together, our studies provide in vivo evidence for targeted recruitment of N-CoR/SMRT-TBLR1 complexes by unliganded TR in transcriptional repression during vertebrate development.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsChromatinDNA-Binding ProteinsHumansLarvaLigandsMacromolecular SubstancesMetamorphosis, BiologicalNuclear ProteinsNuclear Receptor Co-Repressor 2OocytesPromoter Regions, GeneticReceptors, Cytoplasmic and NuclearReceptors, Thyroid HormoneRepressor ProteinsChromatinDNA-Binding ProteinsLigandsMacromolecular SubstancesNCOR2 protein, humanNuclear ProteinsNuclear Receptor Co-Repressor 2nuclear receptor corepressor, XenopusReceptors, Cytoplasmic and NuclearReceptors, Thyroid HormoneRepressor ProteinsTBL1XR1 protein, humanXenopus Proteins

Identifiers

PMID15060155
PMCPMC381683
OpenAlexW2154005091

What OpenQuestion holds

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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.