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The extracellular calcium-sensing receptor (CaSR) is a critical modulator of skeletal development.

Science signaling | Sep 3, 2008

http://www.ncbi.nlm.nih.gov/pubmed/18765830

The extracellular Ca(2+)-sensing receptor (CaSR) plays a nonredundant role in the functions of the parathyroid gland (PTG) and the kidney. Severe hyperparathyroidism, premature death, and incomplete gene excision in Casr(-/-) mice have precluded the assessment of CaSR function in other tissues. We generated mice with tissue-specific deletion of Casr in the PTG, bone, or cartilage. Deletion of Casr in the PTG or bone resulted in profound bone defects, whereas deletion of Casr in chondrocytes (cartilage-producing cells) resulted in death before embryonic day 13 (E13). Mice in which chondrocyte-specific deletion of Casr was induced between E16 and E18 were viable but showed delayed growth plate development. Our data show a critical role for the CaSR in early embryogenesis and skeletal development.

Pubmed ID: 18765830 RIS Download

Mesh terms: Animals | Bone Development | Bone and Bones | Calcium Signaling | Cartilage | Cell Line | Chondrocytes | Embryo Loss | Humans | Insulin-Like Growth Factor I | Mice | Mice, Knockout | Osteoblasts | Parathyroid Glands | Parathyroid Hormone | Receptor, IGF Type 1 | Receptors, Calcium-Sensing

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Associated grants

  • Agency: NIAMS NIH HHS, Id: P01-AR39448
  • Agency: NIA NIH HHS, Id: R01 AG021353
  • Agency: NIA NIH HHS, Id: R01 AG021353-08
  • Agency: NIAMS NIH HHS, Id: R01 AR055924
  • Agency: NIDDK NIH HHS, Id: R01 DK054793
  • Agency: NIA NIH HHS, Id: R01-AG21353
  • Agency: NIAMS NIH HHS, Id: R01-AR050023
  • Agency: NIAMS NIH HHS, Id: R21-AR50662

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