DNA damage-dependent NF-κB activation: NEMO turns nuclear signaling inside out

被引:193
作者
McCool, Kevin W. [2 ,3 ]
Miyamoto, Shigeki [1 ,3 ]
机构
[1] Univ Wisconsin, McArdle Lab Canc Res, Dept Oncol, Wisconsin Inst Med Res 6159, Madison, WI 53705 USA
[2] Univ Wisconsin, Med Scientist Training Program, Madison, WI 53705 USA
[3] Univ Wisconsin, Mol & Cellular Pharmacol Program, Madison, WI 53705 USA
关键词
NF-?B; NEMO; ATM; SUMO; DNA damage; genotoxic stress; PROSTATE-CANCER CELLS; DOUBLE-STRAND BREAKS; RISK MYELODYSPLASTIC SYNDROME; CHAIN ASSEMBLY COMPLEX; ACUTE MYELOID-LEUKEMIA; IONIZING-RADIATION; GENOTOXIC STRESS; BINDING-ACTIVITY; POLYUBIQUITIN CHAINS; CELLULAR SENESCENCE;
D O I
10.1111/j.1600-065X.2012.01101.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The dimeric transcription factor nuclear factor ?B (NF-?B) functions broadly in coordinating cellular responses during inflammation and immune reactions, and its importance in the pathogenesis of cancer is increasingly recognized. Many of the signal transduction pathways that trigger activation of cytoplasmic NF-?B in response to a broad array of immune and inflammatory stimuli have been elaborated in great detail. NF-?B can also be activated by DNA damage, though relatively less is known about the signal transduction mechanisms that link DNA damage in the nucleus with activation of NF-?B in the cytoplasm. Here, we focus on the conserved signaling pathway that has emerged that promotes NF-?B activation following DNA damage. Post-translational modification of NF-?B essential modulator (NEMO) plays a central role in linking the cellular DNA damage response to NF-?B via the ataxia telangiectasia mutated (ATM) kinase. Accumulating evidence suggests that DNA damage-dependent NF-?B activation may play significant biological roles, particularly during lymphocyte differentiation and progression of human malignancies.
引用
收藏
页码:311 / 326
页数:16
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