成肌细胞作为一种未分化的肌肉前体细胞，在肌肉相关疾病的细胞移植治疗上有很大潜力。CDO 信号通路是控制成肌细胞分化的关键调控体系，但其中的的时空调控机制尚未明朗。申请人前期研究发现支架蛋白BNIP-2是CDO信号通路的重要成员。本项目预实验首次发现分子马达蛋白Kinesin5B可以结合并转运BNIP-2，当降低成肌细胞中内源性Kinesin5B时，成肌细胞分化也随之被抑制。提示Kinesin5B是对CDO信号通路进行时空调控并促进成肌细胞分化的新重要因子。本研究拟综合分子生化手段和显微荧光影像技术，深入探索成肌细胞分化过程中Kinesin5B对CDO信号通路的时空调控机制。在此基础上探索利用纳米材料结合成肌细胞移植对肌肉损伤进行修复，并检测在此修复系统中人为干预CDO信号通路的效果。我们的研究有助于阐明肌肉发育的分子机制，为建立肌肉相关疾病防治的新策略提供理论基础。

Myoblast transplantation is a promising method for treating muscle malfunction diseases. CDO pathway is critical for stimulating p38MAPK and modulating myogenic differentiation. However, the temporospatial regulation for CDO pathway is unclear. We reported that scaffold protein BNIP-2 is essential for activating p38MAPK and promoting myogenesis by forming complex with Cdo and JLP. Here we identified the motor protein Kinesin 5B as a novel target of BNIP-2. Myogenic differentiation could be hampered by treating myobalsts with Kinesin5B siRNA, suggesting the important roles of Kinesin5B in myogenesis. Further study will focus on exploring the involvement of Kinesin5B in temporospatial regulation of CDO pathway.We will also try to repair injured mice muscle tissue by using differentiated myoblast embedded on nanofiber scaffold. The effect of modulating CDO pathway on this myoblast-nanofiber repairing system will be tested.