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This Article Accepted manuscript (PDF) Supplementary Data All Versions of this Article: JME-08-0149v1 42/3/215    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wellendorph, P. Articles by Bräuner-Osborne, H. Search for Related Content PubMed PubMed Citation Articles by Wellendorph, P. Articles by Bräuner-Osborne, H.

P Wellendorph, Medicinal chemistry, University of Copenhagen, Copenhagen, 2100, Denmark
L Johansen, University of Copenhagen, Copenhagen, United States
A Jensen, University of Copenhagen, Copenhagen, Denmark
E Casanova, Ludwig Bolzmann Institute for Cancer Research, Vienna, Austria
M Gassmann, Physiology, University of Basel, Basel, Switzerland
P Deprez, Galapagos, Romainville, France
P Clement-Lacroix, Galapagos, Romainville, France
B Bettler, Physiology, University of Basel, Basel, Switzerland
H Bräuner-Osborne, University of Copenhagen, Copenhagen, Denmark

Correspondence: Petrine Wellendorph, Email: pw{at}farma.ku.dk

Abstract

GPRC6A is a seven transmembrane receptor mediating signaling by a wide range of L--amino-acids, a signaling augmented by the divalent cations Ca2+ and Mg2+. GPRC6A transcripts are detected in numerous mammalian tissues, but the physiological role of the receptor is thus far elusive. Analogously to the closely related calcium-sensing receptor, GPRC6A has been proposed to function as a metabolic sensor of Ca2+ and amino acids in bone and other tissues. In the present study, we have generated the first GPRC6A knockout mice and studied their phenotype with particular focus on bone homeostasis. The generated GPRC6A knockout mice are viable and fertile, develop normally and exhibit no significant differences in body weight compared to wild type littermates. Assessment of bone mineral density, histomorphometry and bone metabolism demonstrated no significant differences between 13-week-old knockout and wild type mice. In conclusion, our data do not support a role for GPRC6A in normal bone physiology.

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