A control structure of a nervous system synapse morphosis by a cell adhesion molecule.

果胶是一种钙非依赖性免疫球蛋白样细胞-细胞黏附分子，由四个成员组成。在海马苔藓纤维终末，Nectin-1和Nectin-3分别定位于突触连接的突触前和突触后侧，它们的反式相互作用与N-钙粘素共同参与突触的形成。果胶通过afadin与肌动蛋白细胞骨架联系在一起，afadin是一种与果胶和肌动蛋白细丝结合的蛋白质。抑制Nectin-1-/-小鼠体内基于Nectin-1和Nectin-3的黏附导致突触的异常形成(Honda等人，2006年)。综上所述，很可能是与N-钙粘素共同参与了突触的形成。为了鉴定一个具有细胞聚集活性并参与突触形成的新分子，我们建立了发育海马区的消减文库(P10-P5)。将该文库导入成纤维细胞，进行细胞聚集实验。我们发现电压门控K^+通道是一种细胞黏附分子(Kimura等人，准备提交)。此外，我们还发现水通道水蛋白4具有细胞聚集活性(Hiroaki et al.2006)。

Nectins are Ca^<2+>-independent immunoglobulin-like cell-cell adhesion molecules and comprise a family of four members. At the mossy fiber terminals of hippocampus, nectin-1 and nectin-3 localize at the presynaptic and postsynaptic sides of synaptic junctions, respectively, and their trans-interaction plays a role in formation of synapses in cooperation with N-cadherin. Nectins are associated with the actin cytoskeleton through afadin, a nectin- and actin filament-binding protein. Inhibition of nectin-1-and nectin-3-based adhesion by in nectin-1 -/- mice resulted in the abnormal formation of synapses (Honda et al., 2006). Taken together, it is likely that nectins are involved in the formation of synapses in cooperation with N-cadherin. This role of nectins is consistent with the finding that mutations in the nectin-1 gene are responsible for cleft lip/palate-ectodermal dysplasia, which is characterized by mental retardation in addition to ectodermal dysplasia.For identification of a novel molecule that have cell-aggregation activity and is involved in synapse formation, we made a subtraction library for developmental hippocampus (P10-P5). This library was transfected into fibroblasts and the transfected cells were performed with cell-aggregation assay. We identified a voltage-gated K^+ channel as a cell adhesion molecule (Kimura et al., in preparation for submission). Furthermore, we also found that aquaproin 4, a water channel, has cell aggregation activity (Hiroaki et al. 2006).