ArticleThe EMBO journal2002
Retardation of post-natal development caused by a negatively acting thyroid hormone receptor alpha1.
Article in The EMBO journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
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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.
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Who cites it
52 citing papers in PubMed, 180 citations in OpenAlex.
- Internal diseases and molecular mechanisms causing slipped capital femoral epiphysis in children.World journal of orthopedics · 2025Review
- Impaired thyroid hormone receptor signaling in anterior hypothalamic parvalbumin neurons causes bradycardia in male mice.European thyroid journal · 2025Article
- Sex-specific role of epigenetic modification of a leptin upstream enhancer in adipose tissue.Clinical epigenetics · 2025Article
- Resistance to thyroid hormone induced tachycardia in RTHα syndrome.Nature communications · 2023Article
- Single-cell RNA-based phenotyping reveals a pivotal role of thyroid hormone receptor alpha for hypothalamic development.Development (Cambridge, England) · 2023Article
- Thyroid hormone action during GABAergic neuron maturation: The quest for mechanisms.Frontiers in endocrinology · 2023Review
- Central vs. Peripheral Action of Thyroid Hormone in Adaptive Thermogenesis: A Burning Topic.Cells · 2021Review
- The Clinical Spectrum of Resistance to Thyroid Hormone Alpha in Children and AdultsJournal of clinical research in pediatric endocrinology · 2021Review
- Thyroid Hormone Receptor α Mutations Cause Heart Defects in Zebrafish.Thyroid : official journal of the American Thyroid Association · 2021Article
- A Pivotal Genetic Program Controlled by Thyroid Hormone during the Maturation of GABAergic Neurons.iScience · 2020Article
- Role of thyroid hormones in craniofacial development.Nature reviews. Endocrinology · 2020Review
- Generation of Novel Genetic Models to Dissect Resistance to Thyroid Hormone Receptor α in Zebrafish.Thyroid : official journal of the American Thyroid Association · 2020Article
- Thyroid Hormone Hyposensitivity: From Genotype to Phenotype and Back.Frontiers in endocrinology · 2019Review
- Transport, Metabolism, and Function of Thyroid Hormones in the Developing Mammalian Brain.Frontiers in endocrinology · 2019Review
- Role of Thyroid Hormones in Skeletal Development and Bone Maintenance.Endocrine reviews · 2016Review
- Hippocampal Transcriptome Profile of Persistent Memory Rescue in a Mouse Model of THRA1 Mutation-Mediated Resistance to Thyroid Hormone.Scientific reports · 2016Article
- Resistance to thyroid hormone due to defective thyroid receptor alpha.Best practice & research. Clinical endocrinology & metabolism · 2015Review
- Thyroid hormone receptors and resistance to thyroid hormone disorders.Nature reviews. Endocrinology · 2014Review
- Thyroid hormone receptor α mutation causes a severe and thyroxine-resistant skeletal dysplasia in female mice.Endocrinology · 2014Article
- Resistance to thyroid hormone caused by a mutation in thyroid hormone receptor (TR)α1 and TRα2: clinical, biochemical, and genetic analyses of three related patients.The lancet. Diabetes & endocrinology · 2014Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Most patients with the syndrome resistance to thyroid hormone (RTH) express a mutant thyroid hormone receptor beta (TRbeta) with transdominant negative transcriptional effects. Since no patient with a mutant TRalpha has been identified, we introduced a point mutation into the mouse thyroid hormone receptor (TRalpha1) locus originally found in the TRbeta gene, that reduces ligand binding 10-fold. Heterozygous 2- to 3-week- old mice exhibit a severe retardation of post-natal development and growth, but only a minor reduction in serum thyroxine levels. Homozygous mice died before 3 weeks of age. Adult heterozygotes overcome most of these defects except for cardiac function abnormalities, suggesting that other factors compensate for the receptor defect. However, the additional deletion of the TRbeta gene in this mouse strain caused a 10-fold increase in serum thyroxine, restored hormonal regulation of target genes for TRs, and rescued the growth retardation. The data demonstrate a novel array of effects mediated by a dominant negative TRalpha1, and may provide important clues for identification of a potentially unrecognized human disorder and its treatment.
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Registered trials
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.