The lysosome rupture-activated TAK1-JNK pathway regulates NLRP3 inflammasome activation

Masahiro Okada, Atsushi Matsuzawa, Akihiko Yoshimura, Hidenori Ichijo

Research output: Contribution to journalArticle

68 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)32926-32936
Number of pages11
JournalJournal of Biological Chemistry
Volume289
Issue number47
DOIs
Publication statusPublished - 2014 Nov 21

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Inflammasomes
MAP Kinase Signaling System
Lysosomes
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Rupture
Chemical activation

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology
  • Medicine(all)

Cite this

The lysosome rupture-activated TAK1-JNK pathway regulates NLRP3 inflammasome activation. / Okada, Masahiro; Matsuzawa, Atsushi; Yoshimura, Akihiko; Ichijo, Hidenori.

In: Journal of Biological Chemistry, Vol. 289, No. 47, 21.11.2014, p. 32926-32936.

Research output: Contribution to journalArticle

Okada, Masahiro ; Matsuzawa, Atsushi ; Yoshimura, Akihiko ; Ichijo, Hidenori. / The lysosome rupture-activated TAK1-JNK pathway regulates NLRP3 inflammasome activation. In: Journal of Biological Chemistry. 2014 ; Vol. 289, No. 47. pp. 32926-32936.
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