2009
The calcium-sensing receptor couples to Gαs and regulates PTHrP and ACTH secretion in pituitary cells
Mamillapalli R, Wysolmerski J. The calcium-sensing receptor couples to Gαs and regulates PTHrP and ACTH secretion in pituitary cells. Journal Of Endocrinology 2009, 204: 287-297. PMID: 20032198, PMCID: PMC3777408, DOI: 10.1677/joe-09-0183.Peer-Reviewed Original ResearchConceptsG protein-coupled receptorsACTH secretionCAMP productionProtein-coupled receptorsDifferent G proteinsCaR couplesAtT-20 cellsHormone secretionExtracellular calciumSystemic calcium homeostasisBiological functionsG proteinsBreast cancer cellsCell typesCalcium-sensing receptorCell growthReceptors coupleMalignant breast cellsCancer cellsKidney cellsBreast cellsCAR activationPituitary corticotrophsCalcium homeostasisAnterior pituitary
2003
A Syndrome of Hypocalciuric Hypercalcemia Caused by Autoantibodies Directed at the Calcium-Sensing Receptor
Kifor O, Moore FD, Delaney M, Garber J, Hendy GN, Butters R, Gao P, Cantor TL, Kifor I, Brown EM, Wysolmerski J. A Syndrome of Hypocalciuric Hypercalcemia Caused by Autoantibodies Directed at the Calcium-Sensing Receptor. The Journal Of Clinical Endocrinology & Metabolism 2003, 88: 60-72. PMID: 12519831, DOI: 10.1210/jc.2002-020249.Peer-Reviewed Original ResearchMeSH KeywordsAdultAutoantibodiesBlood Physiological PhenomenaBlotting, WesternCalciumCell LineEnzyme ActivationExtracellular SpaceFemaleHumansHypercalcemiaImmunoglobulinsInositol PhosphatesMiddle AgedMitogen-Activated Protein KinasesParathyroid GlandsParathyroid HormonePedigreePeptide FragmentsReceptors, Calcium-SensingReceptors, Cell SurfaceSyndromeConceptsPTH-dependent hypercalcemiaFamilial hypocalciuric hypercalcemiaHeterozygous inactivating mutationsHypocalciuric hypercalcemiaPTH releaseParathyroid cellsCaR's extracellular domainPatient seraExtracellular amino terminusAnti-CaR antiserumNormocalcemic control subjectsHuman parathyroid cellsBovine parathyroid cellsCalcium-sensing receptorAnti-CAR antibodyCaR-transfected HEK293 cellsInactivating mutationEffect of serumExtracellular domainAntithyroid antibodiesAutoimmune manifestationsEndocrine dysfunctionControl subjectsBlood calciumCaR gene