[Cytokines in bone diseases. Genetic defects of PTH/PTHrP receptor in chondrodysplasia].
Parathyroid hormone-related protein (PTHrP) signaling plays important roles in regulating the differentiation of chondrocytes in endochondral bone development. PTHrP signaling functions as an inhibitory effect on chondrocyte hypertrophy which is a terminal stage of differentiation at a growth plate. Mutations of the PTH÷PTHrP receptor have been identified in Jansen metaphyseal chondrodysplasia, Blomstrand's lethal chondrodysplasia, and enchondromatosis. Furthermore, genetic manipulations of the PTHrP and its receptor genes in mice have demonstrated the critical roles of these proteins in regulating both the switch between proliferation and differentiation of chondrocytes.
Ogata
Naoshi
N
Division of Bone and Cartilage Regenerative Medicine, Division of Tissue Engineering,Faculty of Medicine, the University of Tokyo, Tokyo, Japan.
D000818:Animals; D002454:Cell Differentiation / Q000235:genetics*; D019902:Chondrocytes / Q000166:cytology* / Q000473:pathology; D005097:Exostoses, Multiple Hereditary / Q000235:genetics; D006132:Growth Plate; D006801:Humans; D006984:Hypertrophy; D051379:Mice; D009154:Mutation; D010009:Osteochondrodysplasias / Q000235:genetics; D044162:Parathyroid Hormone-Related Protein / Q000502:physiology*; D044168:Receptor, Parathyroid Hormone, Type 1 / Q000235:genetics* / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology
C473449:PTH1R protein, human; D044162:Parathyroid Hormone-Related Protein; D044168:Receptor, Parathyroid Hormone, Type 1