Sumo regulates neuronal survival and differentiation

在本研究中，我们研究了Necdin的总甲基化和Necdin介导的总甲基化。Necdin在体外被总甲基化，RanBP2的E3连接酶结构域促进了Necdin的总甲基化。Necdin与RanBP2和RanGAP1在神经干细胞的核孔中相互作用。此外，在RanBP2存在的情况下，Necdin和相扑蛋白水解酶的强制共表达降低了总和的RanGAP1水平。这些结果表明，在神经元分化过程中，Necdin调节RanGAP1的苏莫化，从而控制核孔复合体介导的运输。

In this study, we investigated necdin sumoylation and necdin-mediated sumoylation.Necdin is sumoylated in vitro and E3 ligase domain of RanBP2 promoted necdin sumoyaltion. Necdin interacted with RanBP2 and RanGAP1 at nuclear pore in neural stem cells. Furthermore, enforced coexpression of necdin and sumo protease decreased sumoylated RanGAP1 levels in the presence of RanBP2. These results suggest that necdin regulates sumoylation of RanGAP1 to control the nuclear pore complex-mediated transport in neuronal differentiation.