抑癌蛋白Cables1是新发现的一个细胞周期调控蛋白，具有抑制肿瘤的发生、发展的功能，然而目前对于其磷酸化修饰及这些修饰是否影响Cables1蛋白的特性和功能却仍不清楚。本课题组的前期工作首次发现AKT激酶能够磷酸化Cables1蛋白并使14-3-3蛋白与其结合，那么这将如何影响Cables1的蛋白特性和功能？并且这在细胞周期调控和肿瘤发生发展中有什么生物学意义？本研究将采用一系列分子生物学方法和技术，在分子、细胞和动物水平上对这些问题进行一一研究和探讨，这将对阐明抑癌蛋白Cables1的生物学特性和功能提供重要的补充，也将对分析细胞周期的调控机制及肿瘤的发生发展提供重要的线索，因此具有重要的意义和价值。

The tumor suppressor Cables1 is a new protein which can regulate cell cycle and inhibit tumorigenesis. However, it is still unclear to the phosphoryaltion of Cables1 and whether the phosphoryaltion affects the characteristic and function of Calbes1. Our primary work at the first time shows that AKT kinase was ables to phosphorylate Cables1 then recruit 14-3-3 interacting with Cables1. Then how will it affect the characteristic and function of Calbes1? What is it the biological importance in the cell cycle regulation and tumorigenesis? To answer these questions from molecular， cellular and animal level, this project will use a series of molecular biological methods and technologies. It will be a rich complement to understand the biological characteristic and function of Cables1, and also provide the important clue to know the mechanism of cell cycle regulation and tumorigenesis.