Analysis of the molecular mechanism of ER stress regulation by a giant ubiquitin ligase, Apollon

越来越多的重要证据表明，内质网应激诱导的细胞凋亡与神经退行性疾病和糖尿病的发生发展有关。在这项研究中，我们发现Apollon是一种凋亡抑制蛋白，它抑制促凋亡蛋白Bim的表达，并抑制内质网应激依赖的细胞凋亡，而在内质网应激诱导的细胞凋亡过程中，Apollon蛋白的表达减少。此外，我们还证明了Apollon通过促进有丝分裂周期蛋白A的降解在细胞周期调节中发挥关键作用。

There are accumulating important evidences implicating ER stress-inducible apoptosis in the development and progression of neurodegenerative diseases and diabetes. In this study, we have showed that Apollon, which is an inhibitor of apoptosis protein, represses expression of an apoptosis-facilitating protein, Bim, and inhibits ER stress-dependent apoptosis, whereas during ER stress-inducible apoptosis, expression of Apollon protein is decreased. Moreover, we have demonstrated that Apollon plays a critical role in cell-cycle regulation by promoting mitotic cyclin A degradation.