ER stress pathway in apoptosis of DNA damage

本研究旨在阐明内质网应激与DNAdamage细胞死亡的关系，并阐明其作用机制。然而，我们在研究过程中发现，在低氧条件下，γ-Taxin的表达下调，γ-Taxin的蛋白质发生降解。因此，改变了目的，阐明γ-Taxin参与了缺氧引起的细胞死亡。研究发现，细胞死亡是由γ-Taxin的降解引起的。此外，细胞死亡还参与了内质网应激和线粒体途径。

The purpoe of this study was to show that ER stress is related to the cell death of DNAdamage and to elucidate the mechanism. However, We have found thatγ-taxilin is downregulated and protein degradation of γ-taxilin occurs in hypoxia during the research. Therefore, the purpose was changed to clarify thatγ-taxilin is involved in the cell death caused by hypoxia. And it was found that cell death is caused by the degradation of γ-taxilin. In addition, the cell death was participated in the ER stress and mitochondoria pathway.