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

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

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Active Transport, Cell Nucleus
  • Cell Nucleus / metabolism
  • Cytoplasm / metabolism*
  • DNA Mutational Analysis
  • Exportin 1 Protein
  • Gene Expression Regulation, Neoplastic*
  • HEK293 Cells
  • HeLa Cells
  • Humans
  • Karyopherins / metabolism
  • Karyopherins / physiology*
  • Leucine / metabolism
  • Microscopy, Fluorescence / methods
  • Models, Biological
  • NF-kappa B / metabolism*
  • Nuclear Export Signals
  • Oxidation-Reduction
  • Oxidative Stress
  • Receptors, Cytoplasmic and Nuclear / metabolism
  • Receptors, Cytoplasmic and Nuclear / physiology*
  • Signal Transduction
  • Transcription Factors / metabolism*

Substances

  • Karyopherins
  • NF-kappa B
  • NMRAL1 protein, human
  • Nuclear Export Signals
  • Receptors, Cytoplasmic and Nuclear
  • Transcription Factors
  • Leucine