Thyroid hormone receptors

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  • Thyroid hormone receptors (TRs) play a major role in animal physiology. TRs are important and very interesting regulators of diverse aspects, including brain development, hearing, bone growth, morphogenesis, metabolism, intestine, and heart rate in vertebrates (Fig. 1). Aberrant functions of TRs induce tremendous defects in these pathways. For example, the human disease of Resistance to Thyroid Hormone (RTH) (see Chapter 8 by Yoh and Privalsky) is a genetically autosomal dominant inherited syndrome that is caused by mutations in the gene encoding the TRβ.

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  • Thyroid hormone has various effects on cell proliferation, growth and apoptosis. To gain more insight into the molecular dynamics caused by thyroid hormone, gene expression in HeLaTRcells that constitutively over-expressed the thyroid hormone receptor (TR) was analyzed. Gene expression profiling of the HeLaTRcells with an oligonucleotide microarray yielded 229 genes whose expression was significantly altered by T3.

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  • Thyrotropin-releasing hormone receptor (TRHR) has already been cloned in mammals where thyrotropin-releas-inghormone (TRH) isknowntoactasapowerful stimulator of thyroid-stimulating hormone (TSH) secretion. The TRH receptor of amphibians has not yet been characterized, although TRH is specifically important in the adaptation of skin color to environmental changes via the secretion of a-melanocyte-stimulating hormone (a-MSH).

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  • Activating mutations of the thyroid-stimulating hormone receptor (TSHr) have been identified as a cause of toxic adenomas. Germline-inactivating TSHr mutations have beendescribedas a cause of congenital hypothyroidism. The effects of combining activating and inactivating mutations within a single receptor was studied. The double mutant T477I/P639S contained an activating TSHr mutation (P639S) togetherwithan inactivatingone (T477I). Theother one (I486M/P639S) contained two activating mutations.

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  • The thyrotropin receptor (TSHR) undergoes a cleavage at the cell membrane, leading to a heterodimer, comprising an aextracellular and a b-transmembrane and intracellular subunits, held togetherbydisulfidebonds.Moreover, part of the a-subunit of the receptor is shed from thyroid and transfected L cells.To understand the role of cleavage and shedding, we constructed deletion mutants starting, respectively, at the most N-terminal (S314), and C-terminal (L378) cleavage sites previously mapped, corresponding to free b1orb2-subunits without further modification of receptor structure....

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  • Rarely, corticotropin-releasing hormone (CRH) is produced by pancreatic islet tumors, SCLC, medullary thyroid cancer, carcinoids, or prostate cancer. When levels are high enough, CRH can cause pituitary corticotrope hyperplasia and Cushing's syndrome. Tumors that produce CRH sometimes also produce ACTH, raising the possibility of a paracrine mechanism for ACTH production. A distinct mechanism for ACTH-independent Cushing's syndrome involves ectopic expression of various G protein–coupled receptors in the adrenal nodules.

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