| First Author | Chang W | Year | 2008 |
| Journal | Sci Signal | Volume | 1 |
| Issue | 35 | Pages | ra1 |
| PubMed ID | 18765830 | Mgi Jnum | J:180651 |
| Mgi Id | MGI:5306811 | Doi | 10.1126/scisignal.1159945 |
| Citation | Chang W, et al. (2008) The extracellular calcium-sensing receptor (CaSR) is a critical modulator of skeletal development. Sci Signal 1(35):ra1 |
| abstractText | 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. |
