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TRIM13 Positively Regulates the NF-κB Signaling Pathway Induced by Encephalomyocarditis Virus.

Xiaolan Ji1,2, Donglin Bi1,2, Mingqi Liu1,2

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Tripartite motif 13 (TRIM13) enhances Encephalomyocarditis virus (EMCV) infection by promoting NF-κB activation. TRIM13 targets IκBα for non-canonical polyubiquitination, driving inflammation and viral spread.

Keywords:
IκBαencephalomyocarditis virusnuclear factor-κBtripartite motif 13

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Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Encephalomyocarditis virus (EMCV) is a significant pathogen causing encephalomyocarditis.
  • The role of Tripartite Motif 13 (TRIM13) in antiviral immunity against EMCV is unknown.
  • TRIM13 is an effector molecule in innate antiviral immunity.

Purpose of the Study:

  • To investigate the antiviral activity of TRIM13 during EMCV infection.
  • To elucidate the molecular mechanisms by which TRIM13 influences EMCV pathogenesis.
  • To determine TRIM13's role in regulating NF-κB signaling in response to EMCV.

Main Methods:

  • Investigated TRIM13's interaction with IκBα using biochemical assays.
  • Assessed the effect of TRIM13's E3 ubiquitin ligase activity on IκBα phosphorylation.
  • Analyzed IκBα polyubiquitination status using K48- and K63-linked ubiquitin-specific antibodies.
  • Monitored NF-κB nuclear translocation and pro-inflammatory cytokine secretion.

Main Results:

  • TRIM13 was identified as a regulator of NF-κB activation during EMCV infection.
  • TRIM13 directly binds to IκBα and increases its phosphorylation in an E3 ligase-dependent manner.
  • IκBα undergoes polyubiquitination independent of K48 and K63 linkages upon TRIM13 interaction.
  • This process promotes NF-κB nuclear translocation, leading to increased pro-inflammatory cytokine secretion.

Conclusions:

  • TRIM13 facilitates EMCV infection by inducing non-canonical IκBα polyubiquitination and subsequent NF-κB activation.
  • TRIM13 exacerbates inflammatory responses, contributing to viral pathogenesis.
  • TRIM13 represents a potential target for therapeutic intervention against EMCV.