An Inverse Agonist Ligand of the PTH Receptor Partially Rescues Skeletal Defects in a Mouse Model of Jansen's Metaphyseal Chondrodysplasia

Author:

Noda Hiroshi1,Guo Jun1,Khatri Ashok1,Dean Thomas1,Reyes Monica1,Armanini Michael123,Brooks Daniel J123,Martins Janaina S1,Schipani Ernestina4,Bouxsein Mary L123,Demay Marie B1,Potts John T1,Jüppner Harald1,Gardella Thomas J1ORCID

Affiliation:

1. Endocrine Unit, Massachusetts General Hospital, and Harvard Medical School Boston MA USA

2. Department of Orthopedic Surgery, Harvard Medical School Boston MA USA

3. Center for Advanced Orthopedic StudiesBeth Israel Deaconess Medical Center Boston MA USA

4. University of Michigan Ann Arbor MI USA

Funder

National Institute of Arthritis and Musculoskeletal and Skin Diseases

National Institute of Diabetes and Digestive and Kidney Diseases

Publisher

Wiley

Subject

Orthopedics and Sports Medicine,Endocrinology, Diabetes and Metabolism

Reference53 articles.

1. [About atypical chondrodystrophy (achondroplasia) and an as yet unspecified congenital growth disorder of the bony system: metaphyseal dysostosis] Über atypische chondrodystrophie (achondroplasie) und über eine noch nicht beschriebene angeborene wachstumsstörung des knochensystems: metaphysäre dysostosis;Jansen M.;Zeitschrift Orthopädie Chirurgie,1934

2. A Constitutively Active Mutant PTH-PTHrP Receptor in Jansen-Type Metaphyseal Chondrodysplasia

3. Calcium metabolism in the jansen type of metaphyseal dysplasia

4. Hypercalcemia due to constitutive activity of the parathyroid hormone (PTH)/PTH-related peptide receptor: comparison with primary hyperparathyroidism

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