ArticleProceedings of the National Academy of Sciences of the United States of America2013
Nuclear receptor corepressor (NCOR1) regulates in vivo actions of a mutated thyroid hormone receptor α.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 42 citations in OpenAlex.
- Fructose impairs brown adipogenesis by promoting thyroid hormone resistance in differentiated brown adipocytes.Biology open · 2026Article
- The abnormal thyroxine signals triggers podocyte apoptosis in DN mice.In vitro cellular & developmental biology. Animal · 2026Article
- Transcriptional Cofactors for Thyroid Hormone Receptors.Endocrinology · 2025Review
- Nuclear receptor corepressor 1 levels differentially impact the intracellular dynamics of mutant thyroid hormone receptors associated with resistance to thyroid hormone syndrome.Molecular and cellular endocrinology · 2024Article
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
- Mediator subunit MED1 differentially modulates mutant thyroid hormone receptor intracellular dynamics in Resistance to Thyroid Hormone syndrome.Molecular and cellular endocrinology · 2023Article
- Structure-Guided Approach to Relieving Transcriptional Repression in Resistance to Thyroid Hormone α.Molecular and cellular biology · 2022Article
- The Clinical Spectrum of Resistance to Thyroid Hormone Alpha in Children and AdultsJournal of clinical research in pediatric endocrinology · 2021Review
- Persistent COUP-TFII expression underlies the myopathy and impaired muscle regeneration observed in resistance to thyroid hormone-alpha.Scientific reports · 2021Article
- 2021 European Thyroid Association Guideline on Thyroid Disorders prior to and during Assisted Reproduction.European thyroid journal · 2021Article
- Thyroid Hormone Receptor α Mutations Cause Heart Defects in Zebrafish.Thyroid : official journal of the American Thyroid Association · 2021Article
- Genomic and Non-Genomic Mechanisms of Action of Thyroid Hormones and Their Catabolite 3,5-Diiodo-L-Thyronine in Mammals.International journal of molecular sciences · 2020Review
- Multiple mechanisms regulate H3 acetylation of enhancers in response to thyroid hormone.PLoS genetics · 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
- Interplay of fibroblasts with anaplastic tumor cells promotes follicular thyroid cancer progression.Scientific reports · 2019Article
- Genetic and Pharmacological Targeting of Transcriptional Repression in Resistance to Thyroid Hormone Alpha.Thyroid : official journal of the American Thyroid Association · 2019Article
- NCOR1 modulates erythroid disorders caused by mutations of thyroid hormone receptor α1.Scientific reports · 2017Article
- The actions of thyroid hormone signaling in the nucleus.Molecular and cellular endocrinology · 2017Review
- New insights into thyroid hormone action.Pharmacology & therapeutics · 2017Review
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
Abstract
Genetic evidence from patients with mutations of the thyroid hormone receptor α gene (THRA) indicates that the dominant negative activity of mutants underlies the pathological manifestations. However, the molecular mechanisms by which TRα1 mutants exert dominant negative activity in vivo are not clear. We tested the hypothesis that the severe hypothyroidism in patients with THRA mutations is due to an inability of TRα1 mutants to properly release the nuclear corepressors (NCORs), thereby inhibiting thyroid hormone-mediated transcription activity. We crossed Thra1(PV) mice, expressing a dominant negative TRα1 mutant (TRα1PV), with mice expressing a mutant Ncor1 allele (Ncor1(ΔID) mice) that cannot recruit the TR or PV mutant. TRα1PV shares the same C-terminal mutated sequences as those of patients with frameshift mutations of the THRA gene. Remarkably, NCOR1ΔID ameliorated abnormalities in the thyroid-pituitary axis of Thra1(PV/+) mice. The severe retarded growth, infertility, and delayed bone development were partially reverted in Thra1(PV/+) mice expressing NCOR1ΔID. The impaired adipogenesis was partially corrected by de-repression of peroxisome-proliferator activated receptor γ and CCAAT/enhancer-binding protein α gene, due to the inability of TRα1PV to recruit NCOR1ΔID to form a repressor complex. Thus, the aberrant recruitment of NCOR1 by TRα1 mutants could lead to clinical hypothyroidism in humans. Therefore, therapies aimed at the TRα1-NCOR1 interaction or its downstream actions could be tested as potential targets in treating TRα1 mutant-mediated hypothyroidism in patients.
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