Please use this identifier to cite or link to this item:
https://hdl.handle.net/2440/53440
Citations | ||
Scopus | Web of ScienceĀ® | Altmetric |
---|---|---|
?
|
?
|
Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Davey, R. | - |
dc.contributor.author | Turner, A. | - |
dc.contributor.author | McManus, J. | - |
dc.contributor.author | Chiu, W. | - |
dc.contributor.author | Tjahyono, F. | - |
dc.contributor.author | Moore, A. | - |
dc.contributor.author | Atkins, G. | - |
dc.contributor.author | Anderson, P. | - |
dc.contributor.author | Ma, C. | - |
dc.contributor.author | Glatt, V. | - |
dc.contributor.author | MacLean, H. | - |
dc.contributor.author | Vincent, C. | - |
dc.contributor.author | Bouxsein, M. | - |
dc.contributor.author | Morris, H. | - |
dc.contributor.author | Findlay, D. | - |
dc.contributor.author | Zajac, J. | - |
dc.date.issued | 2008 | - |
dc.identifier.citation | Journal of Bone and Mineral Research, 2008; 23(8):1182-1193 | - |
dc.identifier.issn | 0884-0431 | - |
dc.identifier.issn | 1523-4681 | - |
dc.identifier.uri | http://hdl.handle.net/2440/53440 | - |
dc.description.abstract | It 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)2D3]-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. | - |
dc.description.statementofresponsibility | Rachel A Davey, Andrew G Turner, Julie F McManus, WS Maria Chiu, Francisca Tjahyono, Alison J Moore, Gerald J Atkins, Paul H Anderson, Cathy Ma, Vaida Glatt, Helen E MacLean, Cristina Vincent, Mary Bouxsein, Howard A Morris, David M Findlay, Jeffrey D Zajac | - |
dc.language.iso | en | - |
dc.publisher | Amer Soc Bone & Mineral Res | - |
dc.source.uri | http://dx.doi.org/10.1359/jbmr.080310 | - |
dc.subject | Femur | - |
dc.subject | Osteoclasts | - |
dc.subject | Animals | - |
dc.subject | Mice, Inbred C57BL | - |
dc.subject | Mice, Knockout | - |
dc.subject | Mice | - |
dc.subject | Hypercalcemia | - |
dc.subject | Calcium | - |
dc.subject | Calcitriol | - |
dc.subject | Actins | - |
dc.subject | Calcitonin | - |
dc.subject | Acid Phosphatase | - |
dc.subject | Isoenzymes | - |
dc.subject | Integrases | - |
dc.subject | Receptors, Calcitonin | - |
dc.subject | Gene Targeting | - |
dc.subject | Gene Deletion | - |
dc.subject | Phenotype | - |
dc.subject | Female | - |
dc.subject | Male | - |
dc.subject | Tartrate-Resistant Acid Phosphatase | - |
dc.title | Calcitonin receptor plays a physiological role to protect against hypercalcemia in mice | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.1359/JBMR.080310 | - |
pubs.publication-status | Published | - |
dc.identifier.orcid | Atkins, G. [0000-0002-3123-9861] | - |
dc.identifier.orcid | Anderson, P. [0000-0002-8685-3252] | - |
dc.identifier.orcid | Morris, H. [0000-0002-2745-3750] | - |
Appears in Collections: | Aurora harvest Medicine publications |
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.