The role of the proteasome-ubiquitin pathway in regulation of the IFN-γ mediated anti-VSV response in neurons

Jingjun Yang, Derin Tugal, Carol Shoshkes Reiss

Research output: Contribution to journalArticle

Abstract

Pharmacologic inhibition of the proteasome resulted in increased NOS-1 protein levels and increased NO production by neuronal cells. This correlated with an increased antiviral effect of IFN-γ against the replication of vesicular stomatitis virus (VSV) replication in vitro. We also observed that a regulatory protein, Protein Inhibitor of NOS-1 (PIN) was down-regulated by IFN-γ treatment, and more ubiquitinated PIN accumulated in IFN-γ treated neurons. In cells of the reticuloendothelial system, IFN-γ treatment induces the expression of a set of low molecular weight MHC-encoded proteins (LMPs), which replace the β-subunit of the proteasome complex during the proteasome neosynthesis, resulting in a complex termed the immunoproteasome. LMP2, -7, and -10 were induced and the immunoproteasome was generated by IFN-γ treatment in neuronal cells. Importantly, we observed that IFN-γ induced inhibition of VSV protein synthesis was not dependent on ubiquitination.

Original languageEnglish (US)
Pages (from-to)34-45
Number of pages12
JournalJournal of Neuroimmunology
Volume181
Issue number1-2
DOIs
StatePublished - Dec 2006

Keywords

  • NOS-1
  • PIN
  • Ubiquitination
  • VSV

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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