ArticleMolecular and cellular endocrinology2023
Mediator subunit MED1 differentially modulates mutant thyroid hormone receptor intracellular dynamics in Resistance to Thyroid Hormone syndrome.
Article in Molecular and cellular endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- 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
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Thyroid hormone receptor (TR) controls the expression of thyroid hormone (T3)-responsive genes, while undergoing rapid nucleocytoplasmic shuttling. In Resistance to Thyroid Hormone syndrome (RTH), mutant TR fails to activate T3-dependent transcription. Previously, we showed that Mediator subunit 1 (MED1) plays a role in TR nuclear retention. Here, we investigated MED1's effect on RTH mutants using nucleocytoplasmic scoring and fluorescence recovery after photobleaching in transfected cells. MED1 overexpression and knockout did not change the nucleocytoplasmic distribution or intranuclear mobility of C392X and P398R TRα1 at physiological T3 levels. At elevated T3 levels, however, overexpression increased P398R's nuclear retention and MED1 knockout decreased P398R's and A263V's intranuclear mobility, while not impacting C392X. Although A263V TRα1-transfected cells had a high percentage of aggregates, MED1 rescued A263V's impaired intranuclear mobility, suggesting that MED1 ameliorates nonfunctional aggregates. Results correlate with clinical severity, suggesting that altered interaction between MED1 and TRα1 mutants contributes to RTH pathology.
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