Of note, growth hormone in combination with thyroxine to increase IGF1 has not led to significant improvement in height and growth [ 24 ]. Thyroxine therapy suppresses serum TSH levels and increases fT 3 above normal levels. Another potential therapeutic strategy is to develop drugs that enable nuclear receptor co-repressor NCoR to dissociate from unliganded TR or to abrogate the activity of histone deacetylases recruited by NCoR.
Additionally, no mutations in various candidate co-factors involved in TR-mediated transcription were found. It is likely that epigenetic effects that alter the expression of various genes involved in transcription may be involved, although it has not been investigated in these patients so far.
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These observations suggest that genetic and epigenetic modifiers likely play important roles in the phenotypes of affected individuals. The identification of TR mutations as causes for the two forms RTH, elucidation of their mechanism for causing resistance, correlation of genotype with phenotype, and the development of criteria for clinical diagnosis and treatment of RTH provide elegant examples of the convergence of basic, translational, and clinical research to improve the understanding and management of a genetic endocrine disorder.
Pseudohypopara-thyroidism — an example of Seabright's bantam syndrome. Aberrant alternative splicing of thyroid hormone receptor in a TSH-secreting pituitary tumor is a mechanism for hormone resistance. Mol Endocrinol. J Clin Endocrinol Metab. Genome-wide binding patterns of thyroid hormone receptor beta. PLoS One. Mechanisms of thyroid hormone receptor-specific nuclear and extra nuclear actions.
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Expression of mutant thyroid hormone nuclear receptors is associated with human renal clear cell carcinoma. A histone deacetylase inhibitor improves hypothyroidism caused by a TRalpha1 mutant. Hum Mol Genet.
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Related Syndromes of Hormone Resistance on the Hypothalamic-Pituitary-Thyroid Axis
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