The State Key Laboratory of Pharmaceutical Biotechnology, College of Life Sciences, Nanjing University, Nanjing 210093, Peoples Republic of China.
Cell Biol Int. 2012 May 1;36(5):463-8. doi: 10.1042/CBI20110322.
Ro52/SSA is an autoantigen that presents in patients with SS (Sjögren's syndrome) and SLE (systemic lupus erythematosus). It increases cell death and redistributes itself to apoptotic blebs, but its pro-apoptotic function has not been completely identified. Overexpression of Ro52/SSA promoted cell apoptosis induced by DR (death receptor) in caspase-8-dependent manner. Ro52/SSA expression down-regulated c-FLIP(L) [cellular (Fas-associated death domain)-like interleukin 1β-converting enzyme-inhibitory protein long form] expression, and Ro52/SSA siRNAs (small interfering RNAs) increased c-FLIP(L) production, indicating that Ro52/SSA plays a role in c-FLIP(L) regulation. Ro52/SSA negatively regulated c-FLIP(L) transcriptional level probably by suppressing NF-κB (nuclear factor κB) signalling. The data suggest that Ro52/SSA is involved in DR-mediated apoptosis by regulating c-FLIP(L).
Ro52/SSA 是一种自身抗原，存在于干燥综合征 (SS) 和系统性红斑狼疮 (SLE) 患者中。它会增加细胞死亡并重新分布到凋亡小泡中，但它的促凋亡功能尚未完全确定。Ro52/SSA 的过表达以依赖 caspase-8 的方式促进 DR（死亡受体）诱导的细胞凋亡。Ro52/SSA 的表达下调 c-FLIP(L) [细胞 (Fas 相关死亡域)样白细胞介素 1β转化酶抑制蛋白长形式] 的表达，而 Ro52/SSA siRNAs（小干扰 RNA）增加了 c-FLIP(L) 的产生，表明 Ro52/SSA 在 c-FLIP(L) 的调节中发挥作用。Ro52/SSA 通过抑制 NF-κB（核因子 κB）信号转导可能负调控 c-FLIP(L) 的转录水平。这些数据表明，Ro52/SSA 通过调节 c-FLIP(L) 参与 DR 介导的细胞凋亡。
