No evidence for a bone phenotype in GPRC6A knockout mice under normal physiological conditions

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Standard

No evidence for a bone phenotype in GPRC6A knockout mice under normal physiological conditions. / Wellendorph, Petrine; Johansen, Lars Dan; Jensen, Anders Asbjørn; Casanova, Emilio; Gassmann, Martin; Deprez, Pierre; Clément-Lacroix, Philippe; Bettler, Bernhard; Bräuner-Osborne, Hans.

I: Journal of Molecular Endocrinology, Bind 42, Nr. 3, 2009, s. 215-223.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Wellendorph, P, Johansen, LD, Jensen, AA, Casanova, E, Gassmann, M, Deprez, P, Clément-Lacroix, P, Bettler, B & Bräuner-Osborne, H 2009, 'No evidence for a bone phenotype in GPRC6A knockout mice under normal physiological conditions', Journal of Molecular Endocrinology, bind 42, nr. 3, s. 215-223. https://doi.org/10.1677/JME-08-0149

APA

Wellendorph, P., Johansen, L. D., Jensen, A. A., Casanova, E., Gassmann, M., Deprez, P., Clément-Lacroix, P., Bettler, B., & Bräuner-Osborne, H. (2009). No evidence for a bone phenotype in GPRC6A knockout mice under normal physiological conditions. Journal of Molecular Endocrinology, 42(3), 215-223. https://doi.org/10.1677/JME-08-0149

Vancouver

Wellendorph P, Johansen LD, Jensen AA, Casanova E, Gassmann M, Deprez P o.a. No evidence for a bone phenotype in GPRC6A knockout mice under normal physiological conditions. Journal of Molecular Endocrinology. 2009;42(3):215-223. https://doi.org/10.1677/JME-08-0149

Author

Wellendorph, Petrine ; Johansen, Lars Dan ; Jensen, Anders Asbjørn ; Casanova, Emilio ; Gassmann, Martin ; Deprez, Pierre ; Clément-Lacroix, Philippe ; Bettler, Bernhard ; Bräuner-Osborne, Hans. / No evidence for a bone phenotype in GPRC6A knockout mice under normal physiological conditions. I: Journal of Molecular Endocrinology. 2009 ; Bind 42, Nr. 3. s. 215-223.

Bibtex

@article{2419e410f76f11ddbf70000ea68e967b,
title = "No evidence for a bone phenotype in GPRC6A knockout mice under normal physiological conditions",
abstract = "GPRC6A is a seven transmembrane receptor mediating signaling by a wide range of L-alpha-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.",
keywords = "Former Faculty of Pharmaceutical Sciences",
author = "Petrine Wellendorph and Johansen, {Lars Dan} and Jensen, {Anders Asbj{\o}rn} and Emilio Casanova and Martin Gassmann and Pierre Deprez and Philippe Cl{\'e}ment-Lacroix and Bernhard Bettler and Hans Br{\"a}uner-Osborne",
year = "2009",
doi = "10.1677/JME-08-0149",
language = "English",
volume = "42",
pages = "215--223",
journal = "Journal of Molecular Endocrinology",
issn = "0952-5041",
publisher = "BioScientifica Ltd.",
number = "3",

}

RIS

TY - JOUR

T1 - No evidence for a bone phenotype in GPRC6A knockout mice under normal physiological conditions

AU - Wellendorph, Petrine

AU - Johansen, Lars Dan

AU - Jensen, Anders Asbjørn

AU - Casanova, Emilio

AU - Gassmann, Martin

AU - Deprez, Pierre

AU - Clément-Lacroix, Philippe

AU - Bettler, Bernhard

AU - Bräuner-Osborne, Hans

PY - 2009

Y1 - 2009

N2 - GPRC6A is a seven transmembrane receptor mediating signaling by a wide range of L-alpha-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.

AB - GPRC6A is a seven transmembrane receptor mediating signaling by a wide range of L-alpha-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.

KW - Former Faculty of Pharmaceutical Sciences

U2 - 10.1677/JME-08-0149

DO - 10.1677/JME-08-0149

M3 - Journal article

C2 - 19103720

VL - 42

SP - 215

EP - 223

JO - Journal of Molecular Endocrinology

JF - Journal of Molecular Endocrinology

SN - 0952-5041

IS - 3

ER -

ID: 10248157