ArticleProceedings of the National Academy of Sciences of the United States of America2011
Resistance to thyroid hormone is modulated in vivo by the nuclear receptor corepressor (NCOR1).
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- Fructose impairs brown adipogenesis by promoting thyroid hormone resistance in differentiated brown adipocytes.Biology open · 2026Article
- Transcriptional Cofactors for Thyroid Hormone Receptors.Endocrinology · 2025Review
- Nuclear receptor corepressors non-canonically drive glucocorticoid receptor-dependent activation of hepatic gluconeogenesis.Nature metabolism · 2024Article
- Anaplastic thyroid cancer cell-secreted TGFβ1 plays a key role in inducing macrophage polarization of human monocytes.American journal of cancer research · 2024Article
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
- Insights into the function of HDAC3 and NCoR1/NCoR2 co-repressor complex in metabolic diseases.Frontiers in molecular biosciences · 2023Review
- Article
- An H3K4me3 reader, BAP18 as an adaptor of COMPASS-like core subunits co-activates ERα action and associates with the sensitivity of antiestrogen in breast cancer.Nucleic acids research · 2020Article
- Nuclear Receptor Coactivators (NCOAs) and Corepressors (NCORs) in the Brain.Endocrinology · 2020Review
- Genetic and Pharmacological Targeting of Transcriptional Repression in Resistance to Thyroid Hormone Alpha.Thyroid : official journal of the American Thyroid Association · 2019Article
- The Nuclear Receptor-Co-repressor Complex in Control of Liver Metabolism and Disease.Frontiers in endocrinology · 2019Review
- The actions of thyroid hormone signaling in the nucleus.Molecular and cellular endocrinology · 2017Review
- Hereditary 1,25-dihydroxyvitamin D-resistant rickets (HVDRR) caused by aBone reports · 2015Article
- The optimal corepressor function of nuclear receptor corepressor (NCoR) for peroxisome proliferator-activated receptor γ requires G protein pathway suppressor 2.The Journal of biological chemistry · 2015Article
- A novel mutation of thyroid hormone receptor β in exon 10 in a case of thyroid hormone-resistant non-Hodgkin's lymphoma of the thyroid.Oncology letters · 2015Article
- Thyroid hormone receptors and resistance to thyroid hormone disorders.Nature reviews. Endocrinology · 2014Review
- The PPARα-FGF21 hormone axis contributes to metabolic regulation by the hepatic JNK signaling pathway.Cell metabolism · 2014Article
- Thyroid hormone receptor α mutation causes a severe and thyroxine-resistant skeletal dysplasia in female mice.Endocrinology · 2014Article
- A histone deacetylase inhibitor improves hypothyroidism caused by a TRα1 mutant.Human molecular genetics · 2014Article
- Thyroid hormone signaling in vivo requires a balance between coactivators and corepressors.Molecular and cellular biology · 2014Article
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
Mutations in the ligand-binding domain of the thyroid hormone receptor β (TRβ) lead to resistance to thyroid hormone (RTH). These TRβ mutants function in a dominant-negative fashion to interfere with the transcription activity of wild-type thyroid hormone receptors (TRs), leading to dysregulation of the pituitary-thyroid axis and resistance in peripheral tissues. The molecular mechanism by which TRβ mutants cause RTH has been postulated to be an inability of the mutants to properly release the nuclear corepressors (NCORs), thereby inhibiting thyroid hormone (TH)-mediated transcription activity. To test this hypothesis in vivo, we crossed Thrb(PV) mice (a model of RTH) expressing a human TRβ mutant (PV) with mice expressing a mutant Ncor1 allele (Ncor1(ΔID) mice) that cannot recruit a TR or a PV mutant. Remarkably, in the presence of NCOR1ΔID, the abnormally elevated thyroid-stimulating hormone and TH levels found in Thrb(PV) mice were modestly but significantly corrected. Furthermore, thyroid hyperplasia, weight loss, and other hallmarks of RTH were also partially reverted in mice expressing NCOR1ΔID. Taken together, these data suggest that the aberrant recruitment of NCOR1 by RTH TRβ mutants leads to clinical RTH in humans. The present study suggests that therapies aimed at the TR-NCOR1 interaction or its downstream actions could be tested as potential targets in treating RTH.
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