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Petrine Wellendorph, Lars Dan Johansen, Anders A Jensen, Emilio Casanova^1,, Martin Gassmann¹, Pierre Deprez², Philippe Clément-Lacroix², Bernhard Bettler¹

Department of Medicinal Chemistry, Faculty of Pharmaceutical Sciences, University of Copenhagen, Universitetsparken 2, DK-2100 Copenhagen, Denmark¹ Department of Biomedicine, Institute of Physiology, University of Basel, Klingelbergstrasse 50, CH-4056 Basel, Switzerland² Galapagos, 60 Avenue Gaston Roussel, F-93230 Romainville, France

(Correspondence should be addressed to P Wellendorph; Email: pw{at}farma.ku.dk)

(E Casanova is now at Ludwig Boltzmann Institute for Cancer Research (LBI-CR), Währinger Strasse 13a, A-1090 Vienna, Austria)

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 with 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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