期刊
MOLECULAR ENDOCRINOLOGY
卷 21, 期 1, 页码 274-280出版社
ENDOCRINE SOC
DOI: 10.1210/me.2006-0110
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资金
- NATIONAL CANCER INSTITUTE [Z01SC010368] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [ZIADE000380] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL &CRANIOFACIAL RESEARCH [Z01DE000380] Funding Source: NIH RePORTER
- Intramural NIH HHS Funding Source: Medline
Germline knockout of the extracellular Ca2+-sensing receptor (CaR) leads to a phenotype that includes severe hypercalcemia, hyperparathyroidism, relative hypocalciuria, skeletal abnormalities, retarded growth, and early postnatal death. To investigate the role of heterotrimeric G proteins in CaR signaling, we used cre/lox technology to delete the respective alpha-subunits of G(q) and G(11) selectively in parathyroid cells. Mice that were PTH-Cre(+/-); Gnaq(flox/flox); Gna11(-/-) (PTH-G alpha(q)/G(alpha 11)-double knockouts) were viable, but showed all the features of germline knockout of the CaR except hypocalcuria. Our results demonstrate the critical role of both G(q) and G(11) in mediating inhibition of PTH secretion by extracellular Ca2+.
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