Evidence map›Paper›PMID 12446772›Full record

ArticleMolecular and cellular biology2002

Nuclear receptor corepressor recruitment by unliganded thyroid hormone receptor in gene repression during Xenopus laevis development.

Laurent M Sachs, Peter L Jones, Emmanuelle Havis, Nicole Rouse, Barbara A Demeneix, Yun-Bo Shi

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

57 citing papers in PubMed, 95 citations in OpenAlex.

  1. Review
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  6. The ecological function of thyroid hormones.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
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  19. Histone methyltransferase Dot1L is a coactivator for thyroid hormone receptor duringFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    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

6 authors at 4 institutions in 2 countries.

Laurent M SachsUnit 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. sachs@mnhn.fr
Peter L Jones
Emmanuelle Havis
Nicole Rouse
Barbara A Demeneix
Yun-Bo Shi
Laboratoire d’Ethologie Expérimentale et Comparée · FRNational Institutes of Health · USCentre National de la Recherche Scientifique · FREunice Kennedy Shriver National Institute of Child Health and Human Development · 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

Thyroid hormone receptors (TR) act as activators of transcription in the presence of the thyroid hormone (T(3)) and as repressors in its absence. While many in vitro approaches have been used to study the molecular mechanisms of TR action, their physiological relevance has not been addressed. Here we investigate how TR regulates gene expression during vertebrate postembryonic development by using T(3)-dependent amphibian metamorphosis as a model. Earlier studies suggest that TR acts as a repressor during premetamorphosis when T(3) is absent. We hypothesize that corepressor complexes containing the nuclear receptor corepressor (N-CoR) are key factors in this TR-dependent gene repression, which is important for premetamorphic tadpole growth. To test this hypothesis, we isolated Xenopus laevis N-CoR (xN-CoR) and showed that it was present in pre- and metamorphic tadpoles. Using a chromatin immunoprecipitation assay, we demonstrated that xN-CoR was recruited to the promoters of T(3) response genes during premetamorphosis and released upon T(3) treatment, accompanied by a local increase in histone acetylation. Furthermore, overexpression of a dominant-negative N-CoR in tadpole tail muscle led to increased transcription from a T(3)-dependent promoter. Our data indicate that N-CoR is recruited by unliganded TR to repress target gene expression during premetamorphic animal growth, an important process that prepares the tadpole for metamorphosis.

Indexed as

Gene Expression Regulation, DevelopmentalAmino Acid SequenceAnimalsCloning, MolecularGenes, ReporterHindlimbHumansIntestinesLarvaLigandsMetamorphosis, BiologicalMolecular Sequence DataNuclear ProteinsNuclear Receptor Co-Repressor 1OocytesPromoter Regions, GeneticLigandsNCOR1 protein, humanNuclear ProteinsNuclear Receptor Co-Repressor 1nuclear receptor corepressor, XenopusReceptors, Thyroid HormoneRecombinant Fusion ProteinsRepressor ProteinsRNA, MessengerTriiodothyronineXenopus Proteins

Identifiers

PMID12446772
PMCPMC139868
OpenAlexW2140316723

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.