ArticleMolecular endocrinology (Baltimore, Md.)1997
Thyroid hormone resistance syndrome manifests as an aberrant interaction between mutant T3 receptors and transcriptional corepressors.
Article in Molecular endocrinology (Baltimore, Md.), 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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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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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.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 206 citations in OpenAlex.
- 2024 European Thyroid Association Guidelines on diagnosis and management of genetic disorders of thyroid hormone transport, metabolism and action.European thyroid journal · 2024Guideline
- The human THRB thyroid hormone receptor gene and the puzzle of retinal disease phenotypes.Developmental biology · 2026Review
- Nuclear receptor coregulator interactions: beyond the switch.Genes & development · 2026Review
- Persistent COUP-TFII expression underlies the myopathy and impaired muscle regeneration observed in resistance to thyroid hormone-alpha.Scientific reports · 2021Article
- Structural insights revealed by two novel THRB mutations.Endocrine · 2020Article
- Role of thyroid hormones in craniofacial development.Nature reviews. Endocrinology · 2020Review
- Thyroid hormone resistance from newborns to adults: a Spanish experience.Journal of endocrinological investigation · 2019Article
- Mutational Landscape of Resistance to Thyroid Hormone Beta (RTHβ).Molecular diagnosis & therapy · 2019Review
- Assessing the clinical and molecular diagnosis of inherited forms of impaired sensitivity to thyroid hormone from a single tertiary center.Endocrine · 2018Article
- Elevated free thyroxine and non-suppressed thyrotropin.BMJ case reports · 2013Review
- The syndromes of reduced sensitivity to thyroid hormone.Biochimica et biophysica acta · 2013Review
- Nuclear receptor coregulators: modulators of pathology and therapeutic targets.Nature reviews. Endocrinology · 2012Review
- Homozygous thyroid hormone receptor β-gene mutations in resistance to thyroid hormone: three new cases and review of the literature.The Journal of clinical endocrinology and metabolism · 2012Review
- Structural basis for retinoic X receptor repression on the tetramer.The Journal of biological chemistry · 2011Article
- NCoR1 regulates thyroid hormone receptor isoform-dependent adipogenesis.Journal of molecular endocrinology · 2011Article
- Differential recruitment of nuclear coregulators directs the isoform-dependent action of mutant thyroid hormone receptors.Molecular endocrinology (Baltimore, Md.) · 2011Article
- Thyroid hormone receptor mutations in cancer and resistance to thyroid hormone: perspective and prognosis.Journal of thyroid research · 2011Article
- The interaction between nuclear receptor corepressor and histone deacetylase 3 regulates both positive and negative thyroid hormone action in vivo.Molecular endocrinology (Baltimore, Md.) · 2010Article
- Approach to the patient with resistance to thyroid hormone and pregnancy.The Journal of clinical endocrinology and metabolism · 2010Article
- Molecular aspects of thyroid hormone actions.Endocrine reviews · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Nuclear hormone receptors are hormone-regulated transcription factors that play critical roles in chordate development and homeostasis. Aberrant nuclear hormone receptors have been implicated as causal agents in a number of endocrine and neoplastic diseases. The syndrome of Resistance to Thyroid Hormone (RTH) is a human genetic disease characterized by an impaired physiological response to thyroid hormone. RTH is associated with diverse mutations in the thyroid hormone receptor beta-gene. The resulting mutant receptors function as dominant negatives, interfering with the actions of normal thyroid hormone receptors coexpressed in the same cells. We report here that RTH receptors interact aberrantly with a newly recognized family of transcriptional corepressors variously denoted as nuclear receptor corepressor (N-CoR), retinoid X receptor interacting protein-13 (RIP-13), silencing mediator for retinoid and thyroid hormone receptors (SMRT), and thyroid hormone receptor-associating cofactor (TRAC). All RTH receptors tested exhibit an impaired ability to dissociate from corepressors in the presence of thyroid hormone. Two of the RTH mutations uncouple corepressor dissociation from hormone binding; two additional RTH mutants exhibit an unusually strong interaction with corepressor under all hormone conditions tested. Finally, artificial mutants that abolish corepressor binding abrogate the dominant negative activity of RTH mutants. We suggest that an altered corepressor interaction is likely to play a critical role in the dominant negative potency of RTH mutants and may contribute to the variable phenotype in this disorder.
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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.