| Literature DB >> 28363951 |
Murat Bastepe1, Serap Turan2, Qing He3.
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.Entities:
Keywords: G proteins; GNAS; PTH; bone; kidney
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Year: 2017 PMID: 28363951 PMCID: PMC5650080 DOI: 10.1530/JME-16-0221
Source DB: PubMed Journal: J Mol Endocrinol ISSN: 0952-5041 Impact factor: 5.098