我们发现并报道了Erbin是一种可以参与神经损伤再修复的关键蛋白。但是从Erbin 基因彻底敲除的转基因小鼠中无法明确Erbin的具体作用结构域以及Erbin发挥关键作用的高表达组织。Erbin的PDZ结构域是目前认为参与神经修复的关键结构域。我们拟通过Cre-LoxP系统来建立施旺细胞特异性Erbin基因敲除小鼠同时将Erbin的PDZ结构域替换为EGFP荧光蛋白。通过已经在Erbin基因敲除小鼠中建立起来的检测神经损伤再修复能力的系统方法来检测施旺细胞中的Erbin，其PDZ结构域是否为其调节神经损伤再修复的关键结构域，其具体的作用机制如何。为我们更加深入的了解神经损伤再修复、髓鞘再生的具体机制提供新的理论基础，为今后可能出现的基因疗法提供新的靶向蛋白。

We have reported Erbin is required in regulation of remyelination after injury. But The transgenic mice we use is completely knocking out the whole Erbin expression in all tissues. It illustrated a lot of useful information for understanding the working mechanism of nerve recovery after injury. But still we have question: which domain of Erbin is necessary and where Erbin plays its critical role for remyelination. We are going to design one transgenic mice: Erbin-LoxP-PDZ-LoxP-EGFP, which can be crossed with the commercial P0-Cre transgenic mice. Then we will have the transgenic mice P0-ErbinPDZ-/--EGFP, which specifically knock out the PDZ domain of Erbin in Schwann cell and replace it with EGFP fluorescent protein. With the nerve injury animal model we have built up, we can study the exactly working mechanism of Erbin in remyelination.