Format

Send to

Choose Destination
Traffic. 2012 Jun;13(6):790-9. doi: 10.1111/j.1600-0854.2012.01346.x. Epub 2012 Mar 14.

A CRM1-dependent nuclear export signal controls nucleocytoplasmic translocation of HSCARG, which regulates NF-κB activity.

Author information

1
State Key Lab of Protein and Plant Gene Research, School of Life Sciences, Peking University, Beijing 100871, China.

Abstract

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.

[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center