Evidence map›Paper›PMID 12972595›Full record

ArticleMolecular and cellular biology2003

A dominant-negative thyroid hormone receptor blocks amphibian metamorphosis by retaining corepressors at target genes.

Daniel R Buchholz, Shao-Chung Victor Hsia, Liezhen Fu, Yun-Bo Shi

Open access · greenAbstract readComparative Study
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
2.1field-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

75 citing papers in PubMed, 125 citations in OpenAlex.

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  8. Thyroid hormone regulates proximodistal patterning in fin rays.Proceedings of the National Academy of Sciences of the United States of America · 2023
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15 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

4 authors at 1 institution in 1 country.

Daniel R BuchholzUnit on Molecular Morphogenesis, Laboratory of Gene Regulation and Development, National Institute for Child Health and Human Development, Bethesda, Maryland 20892-5431, USA.
Shao-Chung Victor Hsia
Liezhen Fu
Yun-Bo Shi
Eunice 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

The total dependence of amphibian metamorphosis on thyroid hormone (T(3)) provides a unique vertebrate model for studying the molecular mechanism of T(3) receptor (TR) function in vivo. In vitro transcription and developmental expression studies have led to a dual function model for TR in amphibian development, i.e., TRs act as transcriptional repressors in premetamorphic tadpoles and as activators during metamorphosis. We examined molecular mechanisms of TR action in T3-induced metamorphosis by using dominant-negative receptors (dnTR) ubiquitously expressed in transgenic Xenopus laevis. We showed that T(3)-induced activation of T(3) target genes and morphological changes are blocked in dnTR transgenic animals. By using chromatin immunoprecipitation, we show that dnTR bound to target promoters, which led to retention of corepressors and continued histone deacetylation in the presence of T(3). These results thus provide direct in vivo evidence for the first time for a molecular mechanism of altering gene expression by a dnTR. The correlation between dnTR-mediated gene repression and inhibition of metamorphosis also supports a key aspect of the dual function model for TR in development: during T(3)-induced metamorphosis, TR functions as an activator via release of corepressors and promotion of histone acetylation and gene activation.

Indexed as

Gene Expression Regulation, DevelopmentalAcetylationAnimalsAnimals, Genetically ModifiedHistonesIntestinesLarvaMetamorphosis, BiologicalPromoter Regions, GeneticReceptors, Thyroid HormoneRepressor ProteinsTailThyroid HormonesTrans-ActivatorsTranscriptional ActivationTriiodothyronineHistonesReceptors, Thyroid HormoneRepressor ProteinsThyroid HormonesTrans-ActivatorsTriiodothyronineXenopus Proteins

Identifiers

PMID12972595
PMCPMC193935
OpenAlexW2148731017

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.