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

The extracellular calcium-sensing receptor (CaSR) is a critical modulator of skeletal development.
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DOI:
10.1126/scisignal.1159945
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发表时间:
2008-09-02
期刊:
影响因子:
7.3
通讯作者:
Shoback D
Shoback D
中科院分区:
生物学1区
文献类型:
--
作者:
Chang W;Tu C;Chen TH;Bikle D;Shoback D

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细胞外钙敏感受体(Ca 2 + sensing receptor,CaSR)在甲状旁腺(parathyroid gland,PTG)和肾脏的功能中起着重要作用。严重的甲状旁腺功能亢进、过早死亡和Casr−/−小鼠的不完全基因切除排除了对其他组织中CaSR功能的评估。我们产生了在PTG、骨或软骨中具有组织特异性Casr缺失的小鼠。PTG或骨中Casr的缺失导致严重的骨缺损,而软骨细胞(软骨产生细胞)中Casr的缺失导致胚胎第13天(E13)之前的死亡。在E16和E18之间诱导软骨细胞特异性Casr缺失的小鼠存活,但显示生长板发育延迟。我们的数据表明,在早期胚胎发生和骨骼发育的CaSR的关键作用。
The extracellular Ca2+-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.
DOI: 10.1073/pnas.0306141101
发表时间: 2004-04-06
影响因子: 11.1
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