破骨细胞的骨吸收对机体维持正常骨量和骨内微环境稳态至关重要，但其分化的调控机制未完全阐明。Raptor是雷帕霉素靶标蛋白复合物1(mTORC1)的特异组分，在细胞生长与代谢的调节中起重要作用。我们的前期工作发现，髓系细胞(破骨细胞前体)特异敲除Raptor小鼠的破骨细胞分化增加、骨量减少，全基因表达谱分析Raptor缺失的髓系细胞，发现调节破骨细胞分化的重要转录因子NFATc1表达上调，提示Raptor可能抑制NFATc1表达与破骨细胞分化。本课题拟利用髓系细胞特异性敲除Raptor的小鼠和体外诱导髓系细胞破骨分化模型，从分子、细胞和整体水平研究Raptor在破骨细胞分化和骨吸收功能中的作用，探讨Raptor通过调节髓系细胞中NFATc1 表达与转录活性，从而调节破骨细胞分化的分子机制，为破骨细胞分化与骨代谢的调节机制提供新观点，为以破骨细胞为靶点的骨丢失相关疾病防治提供新依据。

The maintenance of adequate bone mass and bone homeostasis is significantly relevant with osteoclast. However, details of mechanisms by which osteoclasts differentiation process is controlled remain ill defined. Regulatory-associated protein of TOR (raptor) is a key component of mTORC1, and plays significant roles in regulation of cell growth and metabolism. Previously, we found that deletion of raptor in myeloid cells (the osteoclast progenitors) promotes osteoclasts differentiation, and subsequently causes bone loss in mice. Besides, we detect myeloid cells lacking of Raptor with Digital Gene Expression Profiling and find NFATc1 expression significantly increased. We speculate raptor would suppress NFATc1 expression and block osteoclast differentiation. In this study, by using specific deletion of raptor in osteoclast progenitors in vivo and in vitro, we aim to investigate the role and molecular mechanisms of raptor in regulating NFATc1 to control osteoclast differentiation and bone resorpotion. Our findings will provide new knowledge for the regulation of osteoclast differentiation and experimental support and potential target for the prevention and treatment of diseases caused by osteoclast defect.