Morphofunctional analyses on the Protein 4. 1-family gene deficient mouse

我们描述了4.1G与膜相关鸟苷酸激酶(MAGUK)家族成员、膜蛋白棕榈酰化6(MPP6)和免疫球蛋白超家族细胞黏附分子CADM4共定位于SLI。在4.1G基因敲除小鼠中，MPP6和CADM4主要定位于雪旺细胞核附近的细胞质中，提示蛋白转运异常。与野生型小鼠相比，4.1G基因敲除的老年小鼠神经的SLI形状发生了改变，表明CADM4对黏附具有功能意义。另一种免疫沉淀实验显示MPP6与4.1G相互作用。这些发现表明，4.1G在靶向MPP6和CADM4靶向SLI方面具有特定的作用，新型的4.1G-MPP6-CADM4膜骨架复合体可能保持了SLI作为抵抗外力的储存库的结构。

We describe that the 4. 1G colocalized at SLI with a member of the membrane-associated guanylate kinase(MAGUK) family, membrane protein palmitoylated 6(MPP6), and an immunoglobulin superfamily-cell adhesion molecule, CADM4. In 4. 1G-knockout mice, both MPP6 and CADM4 were mostly localized in cytoplasm near Schwann cell nuclei, indicating abnormal protein transport. SLI shape was altered in aged 4. 1G-knockout mouse nerves compared to that of wild-type mice, indicating functional significance of CADM4 for adhesion. Another immunoprecipitation experiment revealed that MPP6 was interacting with 4. 1G. These findings indicate that the 4. 1G has a specific role in targeting of MPP6 and CADM4 to the SLI, and the novel 4. 1G-MPP6-CADM4 membrane skeletal complex probably maintains the structure of SLI as a reservoir against external mechanical forces.