Ro52/SSA sensitizes cells to death receptor-induced apoptosis by down-regulating c-FLIP(L)
Ro52/SSA sensitizes cells to death receptor-induced apoptosis by down-regulating c-FLIP(L)
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Ro52/SSA 通过下调 c-FLIP(L) 使细胞对死亡受体诱导的细胞凋亡敏感
DOI：
10.1042/cbi20110322
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发表时间：
2012-05-01
影响因子：
3.9
通讯作者：
Hua, Zi-Chun
中科院分区：
文献类型：
--
作者：
Zhang, Jing;Fang, Lei;Hua, Zi-Chun
Ro 52/SSA是一种自身抗原，存在于SS（干燥综合征）和SLE（系统性红斑狼疮）患者中。它增加细胞死亡并将自身重新分配至凋亡性水泡，但其促凋亡功能尚未完全确定。Ro 52/SSA的过表达可促进DR（死亡受体）诱导的细胞凋亡，并呈caspase-8依赖性。Ro 52/SSA表达下调c-FLIP（L）[细胞（Fas相关死亡结构域）样白细胞介素1 β转化酶抑制蛋白长型]表达，Ro 52/SSA siRNA（小干扰RNA）增加c-FLIP（L）的产生，表明Ro 52/SSA在c-FLIP（L）调节中起作用。Ro 52/SSA可能通过抑制核因子-κ B（nuclear factor kappa B）信号传导负调控c-FLIP（L）的转录水平。这些数据表明Ro 52/SSA通过调节c-FLIP（L）参与DR介导的凋亡。
Ro52/SSA is an autoantigen that presents in patients with SS (Sjogren'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 1 beta-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-kappa B (nuclear factor kappa B) signalling. The data suggest that Ro52/SSA is involved in DR-mediated apoptosis by regulating c-FLIP(L).