The Thyrotropin Receptor

Publisher Summary This chapter discusses the current perceptions of the role of the thyrotropin receptors (TSHR) in disease states. It describes the epitopes of autoantibodies against the TSHR (TSHRAbs)-stimulating TSHRAbs and blocking TSHRAbs, which cause hyper- (Graves' disease) or hypothyroidism idiopathic myxedemal-and will examine the basis for their development. Mutations of the TSHR associated with hyperfunctioning adenomas and will relate these to mutations in the lutropin/choriogonadotropin receptor (LH/CGR) associated with precocious puberty are also described. The complex processes required for thyroid growth and function are regulated by TSHR via a multiplicity of signals, with the aid of and requirement for a multiplicity of hormones that regulate the TSHR via receptor cross-talk: insulin, IGFI, adrenergic receptors, and purinergic receptors. Cross-talk appears to regulate G-protein interactions or activities induced by TSH, as well as TSHR gene expression. The TSHR structure and its mechanism of signal transduction are being rapidly unraveled in several laboratories, since the recent cloning of the receptor.