Journal
CELL REPORTS
Volume 29, Issue 1, Pages 151-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2019.08.072
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Funding
- National Health and Medical Research Council of Australia (NHMRC) [APP1124673, 1117602]
- NHMRC [APP1156455]
- European Research Council (ECFP7-ERC-MICROINNATE)
- Science Foundation Ireland [SFI 12/IA/1531]
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The NLRP3 inflammasome is a cytosolic complex sensing phagocytosed material and various damage-associated molecular patterns, triggering production of the pro-inflammatory cytokines interleukin-1 beta (IL)-1 beta and IL-18 and promoting pyroptosis. Here, we characterize glutathione transferase omega 1-1 (GSTO1-1), a constitutive deglutathionylating enzyme, as a regulator of the NLRP3 inflammasome. Using a small molecule inhibitor of GSTO1-1 termed C1-27, endogenous GSTO1-1 knockdown, and GSTO1-1(-/-) mice, we report that GSTO1-1 is involved in NLRP3 inflammasome activation. Mechanistically, GSTO1-1 deglutathionylates cysteine 253 in NIMA related kinase 7 (NEK7) to promote NLRP3 activation. We therefore identify GSTO1-1 as an NLRP3 inflammasome regulator, which has potential as a drug target to limit NLRP3-mediated inflammation.
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