Cutting Edge: G protein subunit β 1 negatively regulates NLRP3 inflammasome activation

Tomohiko Murakami, Lerdluck Ruengsinpinya, Eriko Nakamura, Yoshifumi Takahata, Kenji Hata, Hiroaki Okae, Shun'ichiro Taniguchi, Masafumi Takahashi, Riko Nishimura

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)

Abstract

The NLRP3 inflammasome has important roles in the pathogenesis of various inflammatory diseases. However, the regulatory mechanisms of the NLRP3 inflammasome are not fully understood. In this study, we attempted to identify molecules that interact with NLRP3 upon its activation. We identified G protein subunit β 1 (GNB1), a downstream molecule of G protein-coupled receptors (GPCRs), which regulates the NLRP3 inflammasome activation. GNB1 was physically associated with NLRP3 via the pyrin domain of NLRP3. Activation of the NLRP3 inflammasome was enhanced in GNB1-knockdown or GNB1-deficient murine macrophages, although a lack of GNB1 did not affect activation of the AIM2 inflammasome. ASC oligomerization induced by NLRP3 was enhanced by GNB1 deficiency. Conversely, NLRP3-dependent ASC oligomerization was inhibited by the overexpression of GNB1. This study indicates that GNB1 negatively regulates NLRP3 inflammasome activation by suppressing NLRP3-dependent ASC oligomerization, and it provides a regulatory mechanism of the NLRP3 inflammasome.

Original languageEnglish
Pages (from-to)1942-1947
Number of pages6
JournalJournal of Immunology
Volume202
Issue number7
DOIs
Publication statusPublished - 2019
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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