ArticleProceedings of the National Academy of Sciences of the United States of America1996
Modulation of the transcriptional activity of thyroid hormone receptors by the tumor suppressor p53.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 81 citations in OpenAlex.
- Epigenomic Modulators and Thyroid Hormone Receptor β Agonists: A New Paradigm for Tumor Suppression in Thyroid Cancer.Endocrinology · 2025Review
- Novel Transcriptional Mechanisms for Regulating Metabolism by Thyroid Hormone.International journal of molecular sciences · 2018Review
- Mitochondria as key targets of cardioprotection in cardiac ischemic disease: role of thyroid hormone triiodothyronine.International journal of molecular sciences · 2015Review
- Mutation analysis underlying the downregulation of the thyroid hormone receptor β1 gene in the Chinese breast cancer population.OncoTargets and therapy · 2015Article
- Characterization of a new mouse p53 variant: loss-of-function and gain-of-function.Journal of biomedical science · 2014Article
- Identification of thyroid hormone receptor active compounds using a quantitative high-throughput screening platform.Current chemical genomics and translational medicine · 2014Article
- The transcription factor p53: not a repressor, solely an activator.Cell cycle (Georgetown, Tex.) · 2014Article
- Thyroid hormone actions in liver cancer.Cellular and molecular life sciences : CMLS · 2013Review
- Oncogenic Actions of the Nuclear Receptor Corepressor (NCOR1) in a Mouse Model of Thyroid Cancer.PloS one · 2013Article
- Small-molecule hormones: molecular mechanisms of action.International journal of endocrinology · 2013Article
- Molecular aspects of thyroid hormone actions.Endocrine reviews · 2010Review
- Molecular characterization of SMILE as a novel corepressor of nuclear receptors.Nucleic acids research · 2009Article
- Regulation of beta-catenin by a novel nongenomic action of thyroid hormone beta receptor.Molecular and cellular biology · 2008Article
- Thyroid hormone receptor-beta (TR beta 1) impairs cell proliferation by the transcriptional inhibition of cyclins D1, E and A2.Oncogene · 2008Article
- The thyroid hormone receptor-alpha (TRalpha) gene encoding TRalpha1 controls deoxyribonucleic acid damage-induced tissue repair.Molecular endocrinology (Baltimore, Md.) · 2008Article
- A single-nucleotide polymorphism in a half-binding site creates p53 and estrogen receptor control of vascular endothelial growth factor receptor 1.Molecular and cellular biology · 2007Article
- Tumour suppressor p53 down-regulates the expression of the human hepatocyte nuclear factor 4alpha (HNF4alpha) gene.The Biochemical journal · 2006Article
- Activation of phosphatidylinositol 3-kinase signaling by a mutant thyroid hormone beta receptor.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- An unliganded thyroid hormone beta receptor activates the cyclin D1/cyclin-dependent kinase/retinoblastoma/E2F pathway and induces pituitary tumorigenesis.Molecular and cellular biology · 2005Article
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Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thyroid hormone nuclear receptors (TRs) are ligand-dependent transcriptional factors that regulate growth, differentiation, and development. The molecular mechanisms by which TRs mediate these effects are unclear. One prevailing hypothesis suggests that TRs may cooperate with other transcriptional factors to mediate their biological effects. In this study, we tested this hypothesis by examining whether the activity of TRs is modulated by the tumor suppressor p53. p53 is a nuclear protein that regulates gene expression via sequence-specific DNA binding and/or direct protein-protein interaction. We found that the human TR subtype beta 1 (h-TR beta 1) physically interacted with p53 via its DNA binding domain. As a result of this physical interaction, binding of h-TR beta 1 to its hormone response elements either as homodimer or as a heterodimer with the retinoic X receptor was inhibited by p53 in a concentration-dependent manner. In transfected cells, wild-type p53 repressed the hormone-dependent transcriptional activation of h-TR beta 1. In contrast, mutant p53 either had no effect or activated the transcriptional activity of h-TR beta 1 depending on the type of hormone response elements. These results indicate the gene regulating activity of TRs was modulated by p53, suggesting that the cross talk between these two transcriptional factors may play an important role in the biology of normal and cancer cells.
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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.