Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Arch Biochem Biophys. 2010 Oct 15;502(2):137-43. doi: 10.1016/j.abb.2010.08.001. Epub 2010 Aug 6.
Selenoprotein K (SelK), an endoplasmic reticulum (ER) resident protein, its biological function has been less-well studied. To investigate the role of SelK in the ER stress response, effects of SelK gene silence and ER stress agents on expression of SelK and cell apoptosis in HepG2 cells were studied. The results showed that SelK was regulated by ER stress agents, Tunicamycin (Tm) and beta-Mercaptoethanol (beta-ME), in HepG2 cells. Moreover, the SelK gene silence by RNA interference could significantly aggravate HepG2 cell death and apoptosis induced by the ER stress agents. These results suggest that SelK is an ER stress-regulated protein and plays an important role in protecting HepG2 cells from ER stress agent-induced apoptosis.
硒蛋白 K（SelK）是一种内质网（ER）驻留蛋白，其生物学功能尚未得到充分研究。为了研究 SelK 在 ER 应激反应中的作用，研究了 SelK 基因沉默和 ER 应激剂对 HepG2 细胞中 SelK 表达和细胞凋亡的影响。结果表明，SelK 受 ER 应激剂，衣霉素（Tm）和β-巯基乙醇（β-ME）调节在 HepG2 细胞中。此外，RNA 干扰使 SelK 基因沉默可显著加重 ER 应激剂诱导的 HepG2 细胞死亡和凋亡。这些结果表明 SelK 是一种 ER 应激调节蛋白，在保护 HepG2 细胞免受 ER 应激剂诱导的细胞凋亡中起重要作用。
