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A CRM 1‐Dependent Nuclear Export Signal Controls Nucleocytoplasmic Translocation of HSCARG , Which Regulates NF‐κB Activity
Author(s) -
Zhang Mei,
Hu Bin,
Li Tingting,
Peng Yanyan,
Guan Junhong,
Lai Shenshen,
Zheng Xiaofeng
Publication year - 2012
Publication title -
traffic
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.677
H-Index - 130
eISSN - 1600-0854
pISSN - 1398-9219
DOI - 10.1111/j.1600-0854.2012.01346.x
Subject(s) - nuclear export signal , chromosomal translocation , cytoplasm , microbiology and biotechnology , biology , nuclear transport , nf κb , cell nucleus , nucleus , nuclear localization sequence , signal transduction , nuclear protein , biochemistry , transcription factor , gene
HSCARG is a newly identified nuclear factor‐κB ( NF‐κB ) 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‐κB activity, we identified a previously uncharacterized nuclear export signal (NES) at residues 272–278 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‐κB by HSCARG. These results indicate that nucleocytoplasmic translocation of HSCARG plays an important role in fine‐tuning NF‐κB signaling.