The PTH-Gαs-protein kinase A cascade controls αNAC localization to regulate bone mass.


The binding of PTH to its receptor induces Gα(s)-dependent cyclic AMP (cAMP) accumulation to turn on effector kinases, including protein kinase A (PKA). The phenotype of mice with osteoblasts specifically deficient for Gα(s) is mimicked by a mutation leading to cytoplasmic retention of the transcriptional coregulator αNAC, suggesting that Gαs and αNAC form… (More)
DOI: 10.1128/MCB.01434-13


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