Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10639
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dc.contributor.authorDavey, Rachel Aen
dc.contributor.authorTurner, Andrew Gen
dc.contributor.authorMcManus, Julie Fen
dc.contributor.authorChiu, W S Mariaen
dc.contributor.authorTjahyono, Franciscaen
dc.contributor.authorMoore, Alison Jen
dc.contributor.authorAtkins, Gerald Jen
dc.contributor.authorAnderson, Paul Hen
dc.contributor.authorMa, Cathyen
dc.contributor.authorGlatt, Vaidaen
dc.contributor.authorMacLean, Helen Een
dc.contributor.authorVincent, Cristinaen
dc.contributor.authorBouxsein, Mary Len
dc.contributor.authorMorris, Howard Aen
dc.contributor.authorFindlay, David Men
dc.contributor.authorZajac, Jeffrey Den
dc.date.accessioned2015-05-16T00:09:33Z
dc.date.available2015-05-16T00:09:33Z
dc.date.issued2008-08-01en
dc.identifier.citationJournal of Bone and Mineral Research : the Official Journal of the American Society For Bone and Mineral Research; 23(8): 1182-93en
dc.identifier.govdoc18627265en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/10639en
dc.description.abstractIt is well established that calcitonin is a potent inhibitor of bone resorption; however, a physiological role for calcitonin acting through its cognate receptor, the calcitonin receptor (CTR), has not been identified. Data from previous genetically modified animal models have recognized a possible role for calcitonin and the CTR in controlling bone formation; however, interpretation of these data are complicated, in part because of their mixed genetic background. Therefore, to elucidate the physiological role of the CTR in calcium and bone metabolism, we generated a viable global CTR knockout (KO) mouse model using the Cre/loxP system, in which the CTR is globally deleted by >94% but <100%. Global CTRKOs displayed normal serum ultrafiltrable calcium levels and a mild increase in bone formation in males, showing that the CTR plays a modest physiological role in the regulation of bone and calcium homeostasis in the basal state in mice. Furthermore, the peak in serum total calcium after calcitriol [1,25(OH)(2)D(3)]-induced hypercalcemia was substantially greater in global CTRKOs compared with controls. These data provide strong evidence for a biological role of the CTR in regulating calcium homeostasis in states of calcium stress.en
dc.language.isoenen
dc.subject.otherAcid Phosphatase.metabolismen
dc.subject.otherActins.metabolismen
dc.subject.otherAnimalsen
dc.subject.otherCalcitonin.blooden
dc.subject.otherCalcitriol.pharmacologyen
dc.subject.otherCalcium.blooden
dc.subject.otherFemaleen
dc.subject.otherFemur.anatomy & histology.pathologyen
dc.subject.otherGene Deletionen
dc.subject.otherGene Targetingen
dc.subject.otherHypercalcemia.metabolism.prevention & controlen
dc.subject.otherIntegrases.metabolismen
dc.subject.otherIsoenzymes.metabolismen
dc.subject.otherMaleen
dc.subject.otherMiceen
dc.subject.otherMice, Inbred C57BLen
dc.subject.otherMice, Knockouten
dc.subject.otherOsteoclasts.drug effects.metabolism.pathologyen
dc.subject.otherPhenotypeen
dc.subject.otherReceptors, Calcitonin.metabolismen
dc.titleCalcitonin receptor plays a physiological role to protect against hypercalcemia in mice.en
dc.typeJournal Articleen
dc.identifier.journaltitleJournal of Bone and Mineral Researchen
dc.identifier.affiliationDepartment of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australiaen
dc.identifier.doi10.1359/jbmr.080310en
dc.description.pages1182-93en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/18627265en
dc.type.austinJournal Articleen
local.name.researcherZajac, Jeffrey D
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptEndocrinology-
crisitem.author.deptMedicine (University of Melbourne)-
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