The DOI matches its Crossref record; 59 of the 59 references it cites were found in a registry or an index.
A20 Restricts Ubiquitination of Pro-Interleukin-1β Protein Complexes and Suppresses NLRP3 Inflammasome Activity
Open accessAbstract
SUMMARY Inappropriate inflammasome activation contributes to multiple human diseases, but the mechanisms by which inflammasomes are suppressed are poorly understood. The NFκB inhibitor A20 is a ubiquitin-modifying enzyme that may prevent human inflammatory diseases and lymphomas. Here, we report that A20-deficient macrophages, unlike normal cells, exhibit spontaneous NLRP3 inflammasome activity to LPS alone. The kinase RIPK3, but not the adaptor MyD88, is required for this response. In normal cells, A20 constitutively associates with caspase-1 and pro-IL-1β, and NLRP3 activation further promotes A20 recruitment to the inflammasome. Pro-IL-1β also co-immunoprecipitates with RIPK1, RIPK3, caspase-1 and caspase-8 in a complex that is modified with K63-linked and unanchored polyubiquitin. In A20-deficient macrophages, this pro-IL-1β-associated ubiquitination is markedly increased in a RIPK3-dependent manner. Mass spectrometric and mutational analyses reveal that K133 of pro-IL-1β is a physiological ubiquitination site that supports processing. Our study reveals a novel mechanism by which A20 prevents inflammatory diseases.
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The role of mitochondria in NLRP3 inflammasome activation
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Metadata
- Authors
- Duong, B. H., Onizawa, M., Oses-Prieto, J. A., Advincula, R., Burlingame, A., Malynn, B. A., & Ma, A.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2015-01
- Volume
- 42
- Issue
- 1
- Pages
- 55-67
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W1981237612
- Cited by
- 273
- References
- 59
- FWCI
- 12.22
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Duong, B. H., Onizawa, M., Oses-Prieto, J. A., Advincula, R., Burlingame, A., Malynn, B. A., & Ma, A. (2015). A20 Restricts Ubiquitination of Pro-Interleukin-1β Protein Complexes and Suppresses NLRP3 Inflammasome Activity. Immunity. https://doi.org/10.1016/j.immuni.2014.12.031
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