抄録
Results: Inhibition of CaMKII, TAK1, or JNK specifically suppressed lysosome rupture-induced NLRP3 inflammasome activation.
Background: The mechanisms underlying lysosome rupture-mediated inflammasome activation are not understood.
Conclusion: Activation of the Ca2+-CaMKII-TAK1-JNK pathway in lysosome rupture is necessary for complete activation of the NLRP3 inflammasome.
Significance: Our results suggest novel roles for the Ca2+-CaMKII-TAK1-JNK pathway in the regulation of the inflammasome and propose potential therapeutic targets for inflammatory diseases.
本文言語 | English |
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ページ(範囲) | 32926-32936 |
ページ数 | 11 |
ジャーナル | Journal of Biological Chemistry |
巻 | 289 |
号 | 47 |
DOI | |
出版ステータス | Published - 2014 11月 21 |
ASJC Scopus subject areas
- 生化学
- 分子生物学
- 細胞生物学