Embryonic stem cells (ESCs) are characterized by their ability to self-renew and their potential to differentiate into any cell type. Therefore, identification of novel molecular markers to verify the pluripotent status of mouse ESCs (mESCs) is of great significance. Kinase D interacting substrate of 220 kDa (Kidins220)/ankyrin repeat-rich membrane spanning (ARMS) plays a crucial role in the integration of growth factor receptor pathways during embryonic development. However, the role of Kidins220/ARMS in ESCs is still unknown. To elucidate the effects of Kidins220/ARMS on ESCs, we performed a knockdown of the Kidins220/ARMS gene by RNA interference. To our surprise, downregulation of Kidins220/ARMS did not alter the pluripotent state of mESCs. In contrast, it was essential for the proliferation and survival of ESCs. Furthermore, downregulation of the ARMS gene limited the migration of embryoid body cells derived from mESCs. This study indicates novel roles of Kidins220/ARMS in ESCs, which may represent valuable targets for future clinical applications of ESCs.

中文翻译：

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Kidins220 / ARMS表达赋予增生作用，但独立于小鼠胚胎干细胞的自我更新。

胚胎干细胞（ESC）的特征在于其自我更新的能力以及分化为任何细胞类型的潜力。因此，鉴定新的分子标记物以验证小鼠ESC（mESC）的多能状态具有重要意义。220 kDa（Kidins220）/锚蛋白重复富集的跨膜（ARMS）的激酶D相互作用底物在胚胎发育过程中生长因子受体途径的整合中起关键作用。但是，Kidins220 / ARMS在ESC中的作用仍然未知。为了阐明Kidins220 / ARMS对ESC的影响，我们通过RNA干扰对Kidins220 / ARMS基因进行了敲除。令我们惊讶的是，Kindins220 / ARMS的下调并没有改变mESC的多能状态。相反，它对于ESC的增殖和存活至关重要。此外，ARMS基因的下调限制了源自mESC的类胚体细胞的迁移。这项研究表明Kidins220 / ARMS在ESC中的新作用，这可能代表了ESC未来临床应用的重要目标。