ArticleMolecular endocrinology (Baltimore, Md.)2009
Thyroid hormone receptor mutations found in renal clear cell carcinomas alter corepressor release and reveal helix 12 as key determinant of corepressor specificity.
Article in Molecular endocrinology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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Who cites it
24 citing papers in PubMed, 34 citations in OpenAlex.
- 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
- Immune-Related Adverse Events as Clinical Biomarkers in Patients with Metastatic Renal Cell Carcinoma Treated with Immune Checkpoint Inhibitors.The oncologist · 2021Article
- Mediator subunit MED1 modulates intranuclear dynamics of the thyroid hormone receptor.Journal of cellular biochemistry · 2020Article
- Mislocalization of Cancer-associated Thyroid Hormone Receptor Mutants.Nuclear receptor research · 2020Article
- Thyroid hormone receptor localization in target tissues.The Journal of endocrinology · 2018Review
- Thyroid hormone suppresses expression of stathmin and associated tumor growth in hepatocellular carcinoma.Scientific reports · 2016Article
- Thyroid Hormones as Renal Cell Cancer Regulators.Journal of signal transduction · 2016Review
- Mutation analysis underlying the downregulation of the thyroid hormone receptor β1 gene in the Chinese breast cancer population.OncoTargets and therapy · 2015Article
- The ability of thyroid hormone receptors to sense t4 as an agonist depends on receptor isoform and on cellular cofactors.Molecular endocrinology (Baltimore, Md.) · 2014Article
- Thyroid hormones, t3 and t4, in the brain.Frontiers in endocrinology · 2014Review
- Thyroid hormone actions in liver cancer.Cellular and molecular life sciences : CMLS · 2013Review
- Genetic features of thyroid hormone receptors.Journal of genetics · 2012Review
- Alternative mRNA splicing of corepressors generates variants that play opposing roles in adipocyte differentiation.The Journal of biological chemistry · 2011Article
- Iodothyronine deiodinases and cancer.Journal of endocrinological investigation · 2011Review
- Mutant thyroid hormone receptors (TRs) isolated from distinct cancer types display distinct target gene specificities: a unique regulatory repertoire associated with two renal clear cell carcinomas.Molecular endocrinology (Baltimore, Md.) · 2011Article
- A mechanism for pituitary-resistance to thyroid hormone (PRTH) syndrome: a loss in cooperative coactivator contacts by thyroid hormone receptor (TR)beta2.Molecular endocrinology (Baltimore, Md.) · 2011Article
- NCoR1 regulates thyroid hormone receptor isoform-dependent adipogenesis.Journal of molecular endocrinology · 2011Article
- Cathepsin H regulated by the thyroid hormone receptors associate with tumor invasion in human hepatoma cells.Oncogene · 2011Article
- Aberrant corepressor interactions implicated in PML-RAR(alpha) and PLZF-RAR(alpha) leukemogenesis reflect an altered recruitment and release of specific NCoR and SMRT splice variants.The Journal of biological chemistry · 2011Article
- Thyroid hormone receptor mutations in cancer and resistance to thyroid hormone: perspective and prognosis.Journal of thyroid research · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Thyroid hormone receptors (TRs) regulate multiple normal physiological and developmental pathways, whereas mutations in TRs can result in endocrine and neoplastic disease. A particularly high rate of TR mutations has been found in human renal clear cell carcinomas (RCCCs). We report here that the majority of these RCCC TR mutants tested are defective for transcriptional activation and behave as dominant-negative inhibitors of wild-type receptor function. Although several of the dominant-negative RCCC TR mutants are impaired for hormone binding, all fail to release from corepressors appropriately in response to T(3), a trait that closely correlates with their defective transcriptional properties. Notably, many of these mutants exhibit additional changes in their specificity for different corepressor splice forms that may further contribute to the disease phenotype. Mapping of the relevant mutations reveals that the C-terminal receptor helix 12 is not simply a hormone-operated switch that either permits or prevents all corepressor binding, but is instead a selective gatekeeper that actively discriminates between different forms of corepressor even in the absence of T(3).
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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.