着丝粒是细胞分裂中已复制染色体组均衡分离的必需结构，调控着纺锤体将染色体牵向两极的动力。CENP-B是保障着丝粒组装的蛋白，INMAP是一种纺锤体蛋白，我们已证明二者互作；INMAP基因沉默可能导致CENP-B断掉DNA结合域、细胞周期时相变化；INMAP过表达导致纺锤体缺陷、细胞分裂阻断、多中心体和多核等。本项目将利用分肽段结合策略，通过Co-IP、Pull down等方法揭示INMAP和CENP-B的具体作用部位；通过蛋白酶及其抑制剂分析INMAP对CENP-B的稳定作用；通过INMAP稳定敲降体系和基因表达芯片、Real-Time RT-PCR、质谱测序和Western blot等分析INMAP与CENP-B的互作改变所致有丝分裂调控相关因子的变化，综合推断INMAP借调节CENP-B介导的着丝粒组装发挥的功能。本研究将对有丝分裂调控机制、特别是其新调控环节的揭示作出贡献。

Centromere is a structure necessary for the replicated genomes to be equilibriously segregated. It regulates the traction power of the spindle to pull chromosomes to the opposite poles. CENP-B is a protein guaranteeing centromere assembly, and INMAP is a spindle protein. We have demonstrated that they may interact with each other. INMAP gene silencing may lead to the loss of the DNA binding domain of CENP-B and cell cycle phase changes. INMAP over expression leads to spindle defects, cell division arrest, and the formation of polycentrosomal and multinucleate cells etc. This project will use segmented protein binding strategy, by the methods such as Co-IP and Pull down, to reveal the precise functional position of INMAP on CENP-B; by use of proteases and their inhibitors, to analyse the stabilizing function of INMAP on CENP-B; by INMAP stably knocked down system and gene expressing chips, Real-Time RT-PCR, mass spectrometric sequencing and Western blot etc., to analyse the changes of mitotic regulation related factors caused by the alteration of the interaction between INMAP and CENP-B. With these efforts to deduce the function of INMAP through the regulation of CENP-B mediated centromere assembly. This study will make a contribution to mitotic regulatory mechanism, especially its new regulatory links.