{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T02:09:17Z","timestamp":1791857357217,"version":"4.3.4"},"reference-count":267,"publisher":"Bioscientifica","issue":"4","content-domain":{"domain":["jme.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2017,5]]},"abstract":"<jats:p>\n                    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 G\n                    <jats:sub>s<\/jats:sub>\n                    and G\n                    <jats:sub>q\/11<\/jats:sub>\n                    . Genetic mutations affecting the activity or expression of the alpha-subunit of G\n                    <jats:sub>s<\/jats:sub>\n                    , encoded by the\n                    <jats:italic>GNAS<\/jats:italic>\n                    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\n                    <jats:italic>GNAS<\/jats:italic>\n                    mutations.\n                  <\/jats:p>","DOI":"10.1530\/jme-16-0221","type":"journal-article","created":{"date-parts":[[2017,3,31]],"date-time":"2017-03-31T20:40:40Z","timestamp":1490992840000},"page":"R203-R224","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-6","source":"Crossref","is-referenced-by-count":47,"title":["Heterotrimeric G proteins in the control of parathyroid hormone actions"],"prefix":"10.1530","volume":"58","author":[{"given":"Murat","family":"Bastepe","sequence":"first","affiliation":[{"name":"1Endocrine UnitDepartment of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Serap","family":"Turan","sequence":"additional","affiliation":[{"name":"2Department of Pediatric EndocrinologyMarmara University School of Medicine, Istanbul, Turkey"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qing","family":"He","sequence":"additional","affiliation":[{"name":"1Endocrine UnitDepartment of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"2017033117402981000_58.4.R203.1","doi-asserted-by":"publisher","DOI":"10.1210\/endo-129-5-2547"},{"key":"2017033117402981000_58.4.R203.2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.7.2732"},{"key":"2017033117402981000_58.4.R203.3","doi-asserted-by":"publisher","DOI":"10.1210\/me.2002-0040"},{"key":"2017033117402981000_58.4.R203.4","first-page":"922","article-title":"Pseudohypoparathyroidism \u2013 an example of \u2018Seabright-Bantam syndrome\u2019","volume":"30","author":"Albright","year":"1942","journal-title":"Endocrinology"},{"key":"2017033117402981000_58.4.R203.5","doi-asserted-by":"publisher","DOI":"10.1002\/ajmg.10751"},{"key":"2017033117402981000_58.4.R203.6","doi-asserted-by":"publisher","DOI":"10.1002\/jor.1100140221"},{"key":"2017033117402981000_58.4.R203.7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.34.20004"},{"key":"2017033117402981000_58.4.R203.8","doi-asserted-by":"publisher","DOI":"10.1086\/320117"},{"key":"2017033117402981000_58.4.R203.9","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/10.12.1231"},{"key":"2017033117402981000_58.4.R203.10","doi-asserted-by":"publisher","DOI":"10.1210\/me.2002-0054"},{"key":"2017033117402981000_58.4.R203.11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200319159"},{"key":"2017033117402981000_58.4.R203.12","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0405091101"},{"key":"2017033117402981000_58.4.R203.13","doi-asserted-by":"publisher","DOI":"10.1038\/ng1560"},{"key":"2017033117402981000_58.4.R203.14","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M307444200"},{"key":"2017033117402981000_58.4.R203.15","doi-asserted-by":"publisher","DOI":"10.1210\/en.2014-1046"},{"key":"2017033117402981000_58.4.R203.16","doi-asserted-by":"publisher","DOI":"10.1172\/JCI32409"},{"key":"2017033117402981000_58.4.R203.17","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.1546"},{"key":"2017033117402981000_58.4.R203.18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.2.999"},{"key":"2017033117402981000_58.4.R203.19","doi-asserted-by":"publisher","DOI":"10.1038\/349117a0"},{"key":"2017033117402981000_58.4.R203.20","unstructured":"Boyce AM Collins MT 1993 Fibrous dysplasia\/McCune-Albright syndrome. 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