In the peripheral nervous system (PNS), Schwann cells (SCs) are required for the myelination of axons. Periaxin (PRX), one of the myelination proteins expressed in SCs, is critical for the normal development and maintenance of PNS. As a member of the ERM (ezrin-radxin-moesin) protein family, ezrin holds our attention since their link to the formation of the nodes of Ranvier. Furthermore, PRX and ezrin are co-expressed in cytoskeletal complexes with periplakin and desmoyokin in lens fiber cells. In the present study, we observed that L-periaxin and ezrin interacted in a "head to head and tail to tail" mode in SC RSC96 through NLS3 region of L-periaxin with F3 subdomain of ezrin interaction, and the region of L-periaxin (residues 1368-1461) with ezrin (residues 475-557) interaction. A phosphorylation-mimicking mutation of ezrin resulted in L-periaxin accumulation on SC RSC96 membrane. Ezrin could inhibit the self-association of L-periaxin, and ezrin overexpression in sciatic nerve injury rats could facilitate the repair of impaired myelin sheath. Therefore, the interaction between L-periaxin and ezrin may adopt a close form to complete protein accumulation and to participate in myelin sheath maintenance.

中文翻译：

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Ezrin通过“头到尾，尾到尾”模式与L-periaxin相互作用，并影响Schwann细胞RSC96中L-periaxin的位置。

在外周神经系统（PNS）中，轴突髓鞘化需要雪旺氏细胞（SCs）。Periaxin（PRX）是SC中表达的髓鞘蛋白之一，对PNS的正常发育和维持至关重要。作为ERM（ezrin-radxin-moesin）蛋白家族的一员，ezrin受到我们的关注，因为它们与Ranvier结的形成有关。此外，PRX和ezrin在晶状体纤维细胞中与周围白蛋白和桥粒芯蛋白在细胞骨架复合物中共表达。在本研究中，我们观察到L-periaxin和ezrin在SC RSC96中以“从头到尾，从尾到尾”的方式通过L-periaxin的NLS3区域与ezrin相互作用的F3子域和L-periaxin区域相互作用。 （残基1368-1461）与ezrin（残基475-557）相互作用。ezrin的磷酸化模拟突变导致L-periaxin积累在SC RSC96膜上。ezrin可以抑制L-periaxin的自缔合，ezrin在坐骨神经损伤大鼠中的过表达可以促进髓鞘受损的修复。因此，L-periaxin与ezrin之间的相互作用可能采取紧密的形式来完成蛋白质的积累并参与髓鞘的维持。