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May 18, 2026Cell Reports0 citationsOpen Access

ISG15 negatively regulates RIPK3-mediated cell death and viral pathogenesis

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YPYi-Chieh PerngJWJessica M.C. WarsawSBSachendra S. Bais

Key Points

  • This research examines how ISG15 regulates RIPK3-mediated necroptosis and its impact on viral infections.
  • Used mice to study the interaction between ISG15 and RIPK3
  • Investigated necroptosis in response to CHIKV infection and various stimuli like TNF and LPS
  • Analyzed the role of ISG15 in controlling inflammation and pathogenesis
  • ISG15 associates with RIPK3 in a RHIM-dependent manner
  • ISG15 limits necroptosis and reduces immunopathology during CHIKV infections
  • Demonstrated a significant modulation of inflammation through ISG15 in various contexts

Abstract

mice. Mechanistically, ISG15 non-covalently associates with the RIPK3 necrosome in an RIP homotypic interaction motif (RHIM)-dependent manner, regulating necroptosis downstream of CHIKV infection, tumor necrosis factor (TNF), lipopolysaccharide (LPS), and poly(I:C) stimulation. These results demonstrate a role for ISG15 in limiting immunopathology during infection by modulating necroptosis-dependent inflammation and pathogenesis.

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Cite This Study

Perng et al. (2026) studied this question.

synapsesocial.com/papers/6a0aac6d5ba8ef6d83b6fce2https://doi.org/10.1016/j.celrep.2026.117360
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