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Key elements involved in the negative regulation of the TSH receptor: G protein-coupled receptor kinases, arrestin and inducible cAMP early repressor

The large family of G protein-coupled receptors (GPCRs) transduces signals of a bewildering variety of extracellular stimuli including hormones, neurotransmitters, ions, cytokines and photons. Many GPCRs undergo a rapid, but reversible decrease or loss of responsiveness upon exposure to their ligand, a phenomenon referred to as homologous desensitization. This process involves an inhibition of the GPCR-interaction with the appropriate G protein and is therefore also coined 'receptor uncoupling'. This rapid form of modulation in responsiveness has to be differentiated from the long-term desensitization caused by transcriptional downregulation (1).

Primarily from studies with rhodopsin and the β-adrenergic receptors, it became apparent that the rapid uncoupling of these GPCRs from the interacting G protein is initiated by phosphorylation of the agonistoccupied, stimulated receptor. Phosphorylation of GPCRs is induced by G protein-coupled receptor kinases (GRKs), a family of serine/threonine kinases with, currently, six known members (2). Once a GPRC is phosphorylated by a

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				L. E. Ericson and M. Nilsson Deactivation of TSH receptor signaling in filter-cultured pig thyroid epithelial cells Am J Physiol Endocrinol Metab, April 1, 2000; 278(4): E611 - E619. [Abstract] [Full Text] [PDF]