The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.
Non-transcriptional Priming and Deubiquitination Regulate NLRP3 Inflammasome Activation
Open accessAbstract
The NLRP3 inflammasome is a key component of the innate immune response to pathogenic infection and tissue damage. It is also involved in the pathogenesis of a number of human diseases, including gouty arthritis, silicosis, atherosclerosis, and type 2 diabetes. The assembly of the NLRP3 inflammasome requires a priming signal derived from pattern recognition or cytokine receptors, followed by a second signal derived from extracellular ATP, pore-forming toxins, or crystalline materials. How these two signals activate the NLRP3 inflammasome is not yet clear. Here, we show that in mouse macrophages, signaling by the pattern recognition receptor TLR4 through MyD88 can rapidly and non-transcriptionally prime NLRP3 by stimulating its deubiquitination. This process is dependent on mitochondrial reactive oxygen species production and can be inhibited by antioxidants. We further show that signaling by ATP can also induce deubiquitination of NLRP3 by a mechanism that is not sensitive to antioxidants. Pharmacological inhibition of NLRP3 deubiquitination completely blocked NLRP3 activation in both mouse and human cells, indicating that deubiquitination of NLRP3 is required for its activation. Our findings suggest that NLRP3 is activated by a two-step deubiquitination mechanism initiated by Toll-like receptor signaling and mitochondrial reactive oxygen species and further potentiated by ATP, which could explain how NLRP3 is activated by diverse danger signals.
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Cites
A role for mitochondria in nlrp3 inflammasome activation
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Self-citationInflammasomes in health and disease
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NLRP3 inflammasome activation: the convergence of multiple signalling pathways on ROS production?
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AIM2 activates the inflammasome and cell death in response to cytoplasmic DNA
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Self-citationSensing and reacting to microbes through the inflammasomes
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Back to the Future with Ubiquitin
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The NLRP3 inflammasome: molecular activation and regulation to therapeutics
Swanson, K. V., Deng, M., & Ting, J. P.-Y. (2019) · Nature Reviews Immunology · doi:10.1038/s41577-019-0165-0 · Cited by 4,884
The NLRP3 Inflammasome: an overview of mechanisms of activation and regulation
Kelley, N., Jeltema, D., Duan, Y., & He, Y. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20133328 · Cited by 3,539
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Broz, P., & Dixit, V. M. (2016) · Nature Reviews Immunology · doi:10.1038/nri.2016.58 · Cited by 3,500
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Metadata
- Authors
- Juliana, C., Fernandes-Alnemri, T., Kang, S., Farias, A., Qin, F., & Alnemri, E. S.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2012-10
- Volume
- 287
- Issue
- 43
- Pages
- 36617-36622
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2082857443
- Cited by
- 773
- References
- 16
- FWCI
- 14.64
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Juliana, C., Fernandes-Alnemri, T., Kang, S., Farias, A., Qin, F., & Alnemri, E. S. (2012). Non-transcriptional Priming and Deubiquitination Regulate NLRP3 Inflammasome Activation. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.m112.407130
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