The Lysosome Rupture-activated TAK1-JNK Pathway Regulates NLRP3 Inflammasome Activation

被引：177

作者：

Okada, Masahiro ^{[1
,2
]}

Matsuzawa, Atsushi ^{[1
,3
]}

Yoshimura, Akihiko ^{[2
]}

Ichijo, Hidenori ^{[1
]}

机构：

[1] Univ Tokyo, Grad Sch Pharmaceut Sci, Lab Cell Signaling, Bunkyo Ku, Tokyo 1130033, Japan

[2] Keio Univ, Sch Med, Dept Microbiol & Immunol, Shinjuku Ku, Tokyo 1608582, Japan

[3] Tohoku Univ, Grad Sch Pharmaceut Sci, Lab Hlth Chem, Aoba Ku, Sendai, Miyagi 9808578, Japan

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2014年 / 289卷 / 47期

基金：

日本学术振兴会;

关键词：

IL-1 SIGNALING PATHWAY; I-KAPPA-B; OXIDATIVE STRESS; KINASE CASCADE; CELL-DEATH; APOPTOSIS; PHOSPHORYLATION; TRANSLOCATION; MITOCHONDRIA; CRYSTALS;

D O I：

10.1074/jbc.M114.579961

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Lysosome rupture triggers NLRP3 inflammasome activation in macrophages. However, the underlying mechanism is not fully understood. Here we showed that the TAK1-JNK pathway, a MAPK signaling pathway, is activated through lysosome rupture and that this activation is necessary for the complete activation of the NLRP3 inflammasome through the oligomerization of an adapter protein, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC). We also revealed that the activation of the TAK1-JNK pathway is sustained through Ca2+ ions and that calcium/calmodulin-dependent protein kinase type II functions upstream of the TAK1-JNK pathway and specifically regulates lysosome rupture-induced NLRP3 inflammasome activation. These data suggest a novel role for the TAK1-JNK pathway as a critical regulator of NLRP3 inflammasome activation.

引用

页码：32926 / 32936

页数：11

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