Molecular mechanism and pathophysiology of nucleophagy induced by cation pump

本研究对人ATP13A4诱导吞核的分子机制和病理生理学进行了研究。我们发现人类ATP13A4没有离子转运功能，其N-末端区域是诱导吞核所必需的。另一方面，小鼠ATP13A4具有阳离子转运功能，不诱导亲核反应。利用DNA芯片和蛋白质组学方法对ATP13A4诱导的噬核相关蛋白进行鉴定。特别是，在表达ATP13A4的细胞中观察到参与蛋白分解系统和细胞应激反应的蛋白表达水平增加。

In this research, the molecular mechanism and pathophysiology of nucleophagy induced by human ATP13A4 were examined. We found that human ATP13A4 had no ion-transporting function and its N-terminal region was essential for induction of nucleophagy. On the other hand, mouse ATP13A4 had cation-transporting function and did not induce nucleophagy. Related proteins for the ATP13A4-induced nucleophagy were identified by DNA microarray and proteomics. Especially, increased expression levels of proteins involved in proteolytic system and cellular stress response were observed in human ATP13A4-expressing cells.