Heterotrimeric G proteins in the control of parathyroid hormone actions. (May 2017)

• Record Type: Journal Article
• Authors: Bastepe, Murat; Turan, Serap; He, Qing
• Is Part Of: Journal of molecular endocrinology. Volume 58:Number 4(2017)
• Page Start: R203
• Page End: R224
• Publication Date: 2017-05
• Subjects: PTH -- G proteins -- GNAS -- bone -- kidney; Molecular endocrinology -- Periodicals; Endocrinology -- Periodicals; 616.407
• DOI: 10.1530/JME-16-0221
• Languages: English
• ISSNs: 0952-5041

Abstract

Abstract : Parathyroid hormone (PTH) is a key regulator of skeletal physiology and calcium and phosphate homeostasis. It acts on bone and kidney to stimulate bone turnover, increase the circulating levels of 1, 25 dihydroxyvitamin D and calcium and inhibit the reabsorption of phosphate from the glomerular filtrate. Dysregulated PTH actions contribute to or are the cause of several endocrine disorders. This calciotropic hormone exerts its actions via binding to the PTH/PTH-related peptide receptor (PTH1R), which couples to multiple heterotrimeric G proteins, including Gs and Gq/11 . Genetic mutations affecting the activity or expression of the alpha-subunit of Gs, encoded by the GNAS complex locus, are responsible for several human diseases for which the clinical findings result, at least partly, from aberrant PTH signaling. Here, we review the bone and renal actions of PTH with respect to the different signaling pathways downstream of these G proteins, as well as the disorders caused by GNAS mutations.