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Department of Biochemistry and Molecular Biology, Institute of Human–Environment Interface Biology, Department of Rehabilitation Medicine, Seoul National University College of Medicine, 103 Daehak‐ro, Jongno‐Gu, Seoul 110‐799, Korea
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Department of Biochemistry and Molecular Biology, Institute of Human–Environment Interface Biology, Department of Rehabilitation Medicine, Seoul National University College of Medicine, 103 Daehak‐ro, Jongno‐Gu, Seoul 110‐799, Korea
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al . 2008 ). Conversely, Cav1 -null mice displayed skeletal muscle abnormalities due to tubular aggregate formation ( Schubert et al . 2007 ) and exercise intolerance ( Razani et al . 2001 ), demonstrating that insulin/IGF signaling depends on the
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IHH-null/Gli3-null mice ( Ehlen et al . 2006 ). IHH binds to aggrecan through its chondroitin sulphate side chains, and in the mouse growth plate normal sulphation of chondroitin sulphate is required for normal IHH protein distribution and signalling
Institut National de la Santé et de la Recherche Médicale U676, Hôpital Robert-Debré, 48 Boulevard Sérurier, F-75019 Paris, France
Department of Physiology and Pharmacology L334, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97201-3098, USA
Institut de Physiologie et Biologie Cellulaires, Centre National de la Recherche Scientifique-Unité Mixte de Recherche, 6187 Pôle Biologie Santé, 40 Avenue du Recteur Pineau, 86022 Poitiers, France
Mental Retardation Research Center, University of California, Neurosciences Research Building, 655 Charles Young Drive South, Los Angeles, California 90095-7088, USA
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Institut National de la Santé et de la Recherche Médicale U676, Hôpital Robert-Debré, 48 Boulevard Sérurier, F-75019 Paris, France
Department of Physiology and Pharmacology L334, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97201-3098, USA
Institut de Physiologie et Biologie Cellulaires, Centre National de la Recherche Scientifique-Unité Mixte de Recherche, 6187 Pôle Biologie Santé, 40 Avenue du Recteur Pineau, 86022 Poitiers, France
Mental Retardation Research Center, University of California, Neurosciences Research Building, 655 Charles Young Drive South, Los Angeles, California 90095-7088, USA
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Institut National de la Santé et de la Recherche Médicale U676, Hôpital Robert-Debré, 48 Boulevard Sérurier, F-75019 Paris, France
Department of Physiology and Pharmacology L334, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97201-3098, USA
Institut de Physiologie et Biologie Cellulaires, Centre National de la Recherche Scientifique-Unité Mixte de Recherche, 6187 Pôle Biologie Santé, 40 Avenue du Recteur Pineau, 86022 Poitiers, France
Mental Retardation Research Center, University of California, Neurosciences Research Building, 655 Charles Young Drive South, Los Angeles, California 90095-7088, USA
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Institut National de la Santé et de la Recherche Médicale U676, Hôpital Robert-Debré, 48 Boulevard Sérurier, F-75019 Paris, France
Department of Physiology and Pharmacology L334, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97201-3098, USA
Institut de Physiologie et Biologie Cellulaires, Centre National de la Recherche Scientifique-Unité Mixte de Recherche, 6187 Pôle Biologie Santé, 40 Avenue du Recteur Pineau, 86022 Poitiers, France
Mental Retardation Research Center, University of California, Neurosciences Research Building, 655 Charles Young Drive South, Los Angeles, California 90095-7088, USA
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Institut National de la Santé et de la Recherche Médicale U676, Hôpital Robert-Debré, 48 Boulevard Sérurier, F-75019 Paris, France
Department of Physiology and Pharmacology L334, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97201-3098, USA
Institut de Physiologie et Biologie Cellulaires, Centre National de la Recherche Scientifique-Unité Mixte de Recherche, 6187 Pôle Biologie Santé, 40 Avenue du Recteur Pineau, 86022 Poitiers, France
Mental Retardation Research Center, University of California, Neurosciences Research Building, 655 Charles Young Drive South, Los Angeles, California 90095-7088, USA
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Institut National de la Santé et de la Recherche Médicale U676, Hôpital Robert-Debré, 48 Boulevard Sérurier, F-75019 Paris, France
Department of Physiology and Pharmacology L334, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97201-3098, USA
Institut de Physiologie et Biologie Cellulaires, Centre National de la Recherche Scientifique-Unité Mixte de Recherche, 6187 Pôle Biologie Santé, 40 Avenue du Recteur Pineau, 86022 Poitiers, France
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compared these data with what we previously observed in PACAP null mice ( Lacombe et al. 2006 ). We show that VIP-deficient males displayed lower serum concentrations of follicle-stimulating hormone (FSH) and a dramatic decrease in the serum
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Endocrinology Unit and EA 1533, University Pierre et Marie Curie, Genetics of Human Reproduction, Hôpital Saint-Antoine, 184 rue de Fg St Antoine, 75012, Paris, France
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LGR4, 5, or 6. Although recent studies using LGR4- and LGR5-null mice indicated the important roles of LGR4 and LGR5 genes in embryonic development and perinatal survival ( Mazerbourg et al. 2004 a , Morita et al. 2004 ), the ligands for these
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, and medial amygdala can completely reverse increased food intake without affecting energy expenditure. Additionally, they show that reactivating MC4R specifically in the PVN in the adult MC4R-null mice causes a mild reduction of body weight ( Balthasar
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null mice, concomitant with dysregulation of pyruvate dehydrogenase. Collectively, these observations suggest that circadian clocks within cardiac and skeletal myocytes significantly influence glucose utilization. Clock-mediated regulation of glucose
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that such differences in the phenotype of deleting GLUT4 could be attributed to the peculiarity of the background strain. In addition, in vitro studies using isolated muscles from the Glut4 null mice exhibited different capacities for insulin
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determined, the clinical symptoms of hypophosphatemia in patients with ARHR are believed to be due to high circulatory levels of FGF23. Dmp-1 null mice have also high circulatory levels of Fgf23, and showed phenotypes resembling ARHR patients ( Feng et al
Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
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Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
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Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
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Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
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retardation, as assessed by body length and femoral length, as well as a significant reduction in femoral vBMD ( Yakar et al. 2002 a , 2002 b ). Interestingly, Igf1 null mice also exhibit a cortical phenotype similar to LA mice, but have increased
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osteoblasts from calvaria. At variance with our data, Sun et al. (2003) reported no role for ghrelin in the maintenance of bone density since ghrelin-null mice had normal bone mineral density and bone mineral content. Interestingly enough, food