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RING1 negatively regulates pyroptosis by ubiquitination of Gasdermin D (GSDMD), impacting host defense against bacterial infections and sepsis. Loss of RING1 increases susceptibility to pathogens and inflammation.

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Area of Science:

  • Molecular Biology
  • Immunology
  • Cellular Biology

Background:

  • RING1, an E3 ligase in Polycomb Repressive Complex 1 (PRC1), regulates chromatin and cellular processes.
  • The role of RING1 in inflammation and pyroptosis, a programmed cell death pathway, is not well understood.

Purpose of the Study:

  • To investigate the role of RING1 in regulating pyroptosis and host defense against bacterial infections.
  • To elucidate the molecular mechanism by which RING1 influences Gasdermin D (GSDMD) activity.

Main Methods:

  • In vivo studies using mouse models of bacterial infection (S. typhimurium, M. tuberculosis) and sepsis (LPS-induced).
  • Biochemical assays to determine RING1-GSDMD interaction and ubiquitination sites (K51, K168).
  • Analysis of GSDMD levels, pyroptosis, and immune responses in Ring1 knockout models.

Main Results:

  • RING1 promotes K48-linked ubiquitination of GSDMD, targeting it for proteasomal degradation and inhibiting pyroptosis.
  • Loss of RING1 enhances susceptibility to S. typhimurium infection and exacerbates LPS-induced sepsis.
  • While initially reducing M. tuberculosis load, RING1 deletion leads to increased lung inflammation and impaired immunity.

Conclusions:

  • RING1 acts as a crucial negative regulator of GSDMD-mediated pyroptosis and inflammatory responses.
  • RING1 influences host susceptibility to bacterial pathogens and sepsis.
  • RING1 represents a potential therapeutic target for infectious diseases.