Endocrine Abstracts

The mechanisms controlling the timing of puberty remain largely unknown. Recent insights into genetic causes of pubertal disorders have provided important advances in our understanding of the physiology underlying this developmental process. Mutations in genes important in neuroendocrine pathways controlling GnRH release and LH and FSH secretion have been identified in patients with isolated hypogonadotropic hypogonadism, Kallmann syndrome, and central precocious puberty. Many...

Signaling by TSH receptor (TSHR) was thought to terminate after withdrawal of TSH. Recently, however, TSHR was found to signal persistently even after TSH withdrawal via both the cAMP and inositol-1,4,5-trisphosphate pathways. Similar persistent signaling was found for other G protein-coupled receptors, such as the parathyroid hormone receptor, which stimulates the cAMP pathway, and the S1P1 receptor, which inhibits the cAMP pathway. For TSHR, a controversy has developed as to...

The classical model of GPCR activation entails the binding of a single ligand to a single receptor molecule, followed by transmembrane signal transduction to the appropriate G protein(s). The possibility of GPCRs functioning as dimers or oligomers still remains controversial, and is largely based on in vitro studies on transfected cells. The glycoprotein hormone receptors, including that of LH (LHCGR), differ from most GPCRs by their large extracellular ligand-binding...

The LH receptor (LHR) together with the FSH receptor (FSHR) and TSH receptor (TSHR) constitute a highly conserved subgroup of G protein-coupled receptors. Activation of these receptors requires the binding of the glycoprotein hormones to the long and divergent N-terminus of the receptor and the intramolecular signal transduction from the hormone-receptor complex to the transmembrane domain of the receptor. The main signaling pathway of the LHR, TSHR and FSHR is stimulation of ...