USP4 positively regulates RIG-I-mediated antiviral response through deubiquitination and stabilization of RIG-I

J Virol. 2013 Apr;87(8):4507-15. doi: 10.1128/JVI.00031-13. Epub 2013 Feb 6.

Abstract

Protein ubiquitination plays an essential role in the regulation of retinoic acid-inducible gene I (RIG-I) activation and the antiviral immune response. However, the function of the opposite process of deubiquitination in RIG-I activation remains elusive. In this study, we have identified the deubiquitinating enzyme ubiquitin-specific protease 4 (USP4) as a new regulator for RIG-I activation through deubiquitination and stabilization of RIG-I. USP4 expression was attenuated after virus-induced RIG-I activation. Overexpression of USP4 significantly enhanced RIG-I protein expression and RIG-I-triggered beta interferon (IFN-β) signaling and, at the same time, inhibited vesicular stomatitis virus (VSV) replication. Small interfering RNA (siRNA) knockdown of USP4 expression had an opposite effect. Furthermore, USP4 was found to interact with RIG-I and remove K48-linked polyubiquitination chains from RIG-I. Therefore, we identified USP4 as a new positive regulator for RIG-I that acts through deubiquitinating K48-linked ubiquitin chains and stabilizing RIG-I.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line
  • DEAD Box Protein 58
  • DEAD-box RNA Helicases / immunology
  • DEAD-box RNA Helicases / metabolism*
  • Humans
  • Proteolysis
  • Receptors, Immunologic
  • Ubiquitin / metabolism*
  • Ubiquitin Thiolesterase / immunology
  • Ubiquitin Thiolesterase / metabolism*
  • Ubiquitin-Specific Proteases
  • Vesiculovirus / immunology
  • Vesiculovirus / physiology
  • Virus Replication

Substances

  • Receptors, Immunologic
  • USP4 protein, human
  • Ubiquitin
  • Ubiquitin Thiolesterase
  • Ubiquitin-Specific Proteases
  • RIGI protein, human
  • DEAD Box Protein 58
  • DEAD-box RNA Helicases