甲状旁腺素（Parathyroid Hormone,PTH）促进骨形成的机理有待进一步深入研究。我们的前期研究提示，在PTH诱发的多个信号通路中，磷脂酶C（PLC）非依赖蛋白激酶C（PKC）激活信号通路（PTH/nonPLC/PKC）在促进骨形成，改善骨微结构中起着重要的作用。但PTH/nonPLC/PKC的具体信号中介分子和相应的生物学机制尚不清楚。我们拟以PKC激活检测的荧光能量共振转移（FRET）报告体系为工具，利用PLC缺陷的PTH受体，分析PTH/nonPLC/PKC信号介导途径；设计和筛选nonPLC/PKC特异性PTH模拟肽，并明确其在骨代谢中的功能；分析PTH/nonPLC/PKC的效应分子，筛选该信号通路的作用靶点。目的：阐明PTH/nonPLC/PKC的信号转导机制及其在骨代谢中的功能，优化PTH模拟肽的设计和研究，为设计新的基于PTH的更有效促骨形成药物提供理论依据。

The mechanism that Parathyroid Hormone (PTH) enhances bone formation needs to be further studied. Our previous study revealed that in the versatile signaling pathways induced by PTH, the PLC-independent PKC pathway (PTH/nonPLC/PKC) plays a significant role in bone formation and micro-structural reinforcement.However the pathways that compose PTH/nonPLC/PKC signaling and its biological functions remains unkown. We propose: to screen the possible signaling pathways that mediated PTH/nonPLC/PKC, with fluorescence resonance energy transfer (FRET) technique and PLC-deficit PTH receptor; to design and screen nonPLC/PKC specific PTH analogs, and analyze their functions in bone metabolism; to sort out effective molecules that downsteam PTH/nonPLC/PKC, and find the targets of PTH/nonPLC/PKC signaling. Aim: to understand the mechanism of PTH/nonPLC/PKC signaling pathway and its biological functions in bone metabolism; optimize the designation and study of signaling selective PTH analogs; to provide new theoretic information for new PTH signaling selective analogs designation thus could upgrade PTH's bone formation effect.