A CRM1-Dependent Nuclear Export Signal Controls Nucleocytoplasmic Translocation of HSCARG, Which Regulates NF-?B Activity | |
Zhang, Mei ; Hu, Bin ; Li, Tingting ; Peng, Yanyan ; Guan, Junhong ; Lai, Shenshen ; Zheng, Xiaofeng | |
2012 | |
关键词 | CRM1 HSCARG NF-?B nuclear export signal oxidative stress KAPPA-B UBIQUITIN-LIGASE OXIDATIVE STRESS LOCALIZATION SIGNAL SENSOR PROTEIN DNA-BINDING CELL-DEATH TRANSPORT CRM1 ACTIVATION |
DOI | 10.1111/j.1600-0854.2012.01346.x |
英文摘要 | HSCARG is a newly identified nuclear factor-?B (NF-?B) inhibitor that plays important roles in cell growth. Our previous study found that HSCARG could shuttle between the nucleus and cytoplasm by sensing the change in cellular redox states. To further investigate the mechanism of HSCARG translocation and its effect on the regulation of NF-?B activity, we identified a previously uncharacterized nuclear export signal (NES) at residues 272278 of HSCARG that is required for its cytoplasmic translocation. This leucine-rich NES was found to be mediated by chromosome region maintenance 1. More importantly, accumulation of HSCARG in the nucleus occurred following a mutation in the NES or oxidative stress, which attenuated the inhibition of NF-?B by HSCARG. These results indicate that nucleocytoplasmic translocation of HSCARG plays an important role in fine-tuning NF-?B signaling.; Cell Biology; SCI(E); PubMed; 3; ARTICLE; 6; 790-799; 13 |
语种 | 英语 |
内容类型 | 期刊论文 |
源URL | [http://ir.pku.edu.cn/handle/20.500.11897/194393] |
专题 | 生命科学学院 |
推荐引用方式 GB/T 7714 | Zhang, Mei,Hu, Bin,Li, Tingting,et al. A CRM1-Dependent Nuclear Export Signal Controls Nucleocytoplasmic Translocation of HSCARG, Which Regulates NF-?B Activity[J],2012. |
APA | Zhang, Mei.,Hu, Bin.,Li, Tingting.,Peng, Yanyan.,Guan, Junhong.,...&Zheng, Xiaofeng.(2012).A CRM1-Dependent Nuclear Export Signal Controls Nucleocytoplasmic Translocation of HSCARG, Which Regulates NF-?B Activity.. |
MLA | Zhang, Mei,et al."A CRM1-Dependent Nuclear Export Signal Controls Nucleocytoplasmic Translocation of HSCARG, Which Regulates NF-?B Activity".(2012). |
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