Aberrant production of amyloid beta (Aβ) causes disruption of intracellular calcium homeostasis, a crucial factor in the pathogenesis of Alzheimer's disease. Calcium is required for the fusion and trafficking of vesicles. Previously, we demonstrated that Sec31A, a main component for coat protein complex II (COPII) vesicles at ER exit sites (ERES), is modulated by O‐GlcNAcylation. O‐GlcNAcylation, a unique and dynamic protein glycosylation process, modulates the formation of COPII vesicles.

中文翻译：

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淀粉样蛋白β通过钙稳态紊乱引发的O-GlcNAcylation调节ER出口位点的形成

淀粉样蛋白 β (Aβ) 的异常产生导致细胞内钙稳态的破坏，这是阿尔茨海默病发病机制中的一个关键因素。囊泡的融合和运输需要钙。此前，我们证明了 Sec31A 是内质网出口位点 (ERES) 外壳蛋白复合物 II (COPII) 囊泡的主要成分，受 O-GlcNAcylation 调节。O-GlcNAcylation 是一种独特且动态的蛋白质糖基化过程，可调节 COPII 囊泡的形成。