Interferon regulatory factor 5, a novel mediator of cell cycle arrest and cell death.
Interferon regulatory factor 5, a novel mediator of cell cycle arrest and cell death.
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发表时间：
2003-10
期刊：
影响因子：
11.2
通讯作者：
B. Barnes;M. Kellum;Karen E Pinder;J. Frisancho;P. Pitha
中科院分区：
文献类型：
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作者：
B. Barnes;M. Kellum;Karen E Pinder;J. Frisancho;P. Pitha
我们以前已经证明了干扰素调节因子5(IRF-5)在对病毒感染的先天性免疫反应中起着关键作用。我们首次发现，尽管IRF-5是P53的直接靶点，但它的细胞周期调节和促凋亡作用不依赖于P53。在缺乏野生型P53的情况下，IRF-5在体外和体内都能抑制B细胞淋巴瘤肿瘤的生长。IRF-5介导的生长抑制的分子机制(S)与G(2)-M细胞周期停滞以及p21、Bak、DAP kinase2和bax等生长调节和促凋亡基因的调控有关。综上所述，这些数据表明，尽管IRF-5是P53的下游靶点，但它的生长抑制和促凋亡作用不依赖于P53。
We have previously shown a critical role for IFN regulatory factor 5 (IRF-5) in the innate immune response to virus infection. For the first time, we now show that although IRF-5 is a direct target of p53, its cell cycle regulatory and proapoptotic effects are p53 independent. IRF-5 inhibits both in vitro and in vivo B-cell lymphoma tumor growth in the absence of wild-type p53. The molecular mechanism(s) of IRF-5-mediated growth inhibition is associated with a G(2)-M cell cycle arrest and modulation of growth regulatory and proapoptotic genes, including p21, Bak, DAP kinase 2, and Bax. Taken together, these data indicate that although IRF-5 is a downstream target of p53, its growth inhibitory and proapoptotic effects are independent of p53.