Stress granules and inflammasomes are intracellular complexes that assemble in response to cellular stress signals,enabling cells to persist and perish,respectively.In a recent study published in Nature,Samir et al.id...
In the initial published version of this article,there was a mistake in the title.The correct title should be "Mitochondrial DNA synthesis fuels NLRP3 activation".This correction does not affect the description of the...
Mitochondria-derived signals are associated with NLRP3 inflammasome activation. A recent study in Nature by Zhong et al. shows that inflammasome priming drives new mito- chondrial DNA synthesis, and proposes this to b...
Inflammasome sensors recognize pathogens and danger signals and assemble an immune signaling com- plex, which induces the secretion of pro-inflammatory cytokines IL-1β and IL-18, and pyroptosis. A new study published...
Chemotherapies are known often to induce severe gastrointestinal tract toxicity but the underlying mechanism re- mains unclear. This study considers the widely applied cytotoxic agent irinotecan (CPT-11) as a repres...
The protein kinase R (PKR) functions in the antiviral response by controlling protein translation and inflamma- tory cell signaling pathways. We generated a transgenic, knock-in mouse in which the endogenous PKR is ...
Inflammasomes control host cell death and inflammation in response to sterile or infectious stimuli. Two recent reports published in Science reveal the structural basis for the assembly of NAIP-NLRC4 inflammasomes.
Inflammasome is an intracellular signaling complex of the innate immune system. Activation of inflammasomes promotes the secretion of interleukin 1β (IL-Iβ) and IL-18 and triggers pyroptosis. Caspase-1 and -11 (o...
We thank Dr Warren Strober (National Institutes of Health, USA) for providing the Nlrp3-deficient mice, Dr Vishva Dixit (Genentech, Inc., USA) for providing Asc-deficient mice, Dr Jfirg Tschopp (University of Lausanne, Switzerland) for provid- ing shRNA constructs. We also thank Dr Xudong Zhu (Nankai University, China) for helpful discussion and our colleague Ms Cuili Dong for excellent technical assistance. This work was sup- ported by grants from 100 Talent Program of the Chinese Acad-emy of Sciences, the National Natural Science Foundation of China (91029707, 31170868, 812111134, 31100622), Shanghai Natural Science Foundation (11ZR1442600), Novo Nordisk-CAS Research Foundation, SA-SIBS Scholarship Program, Chinese Postdoctoral Science Foundation (20110490752) and Postdoctoral Research Foundation of Shanghai Institutes for Biological Sci- ences (2011 KIP513), as well as grants from the National Key Ba- sic Research Program (2013CB531600) and National Science and Technology Major Project (2012ZX 10002007-003) of China.
Dear Editor, Many opportunistic fungi are devastating pathogens that cause lethal infection. Cryptococcus neoformans (C. neoformans) is such a fungus that mainly infects im- munocompromised hosts such as AIDS patie...
We thank R Caspi (National Eye Institute, NIH, USA) and D Li (Shanghai Institutes for Biological Sciences, China) for helpful comments, and S Skinner for critical reading of the manuscript. This work was supported by the National Basic Research Program of China (973 program, 2013CB530504), the National Natural Science Foundation of China (31230024, 31030029, 31100662, 31030023, 91029707, 31170868), the Shanghai Natural Science Foundation (11ZR1442600), the National Ministry of Science and Technology (2007DFC31700), the National Science and Technology Major Project (2008ZX10004-002, 2008ZX10002-014, 2009ZX10004-105, 2009ZXI0004-016, 2011ZX10004-001 and 2012ZXl0002007), the Shanghai Pasteur Health Research Foundation (SPHRF2008001 and SPHRF2009001), the SA-SIBS Discovery Innovation Grant, the Li Kha Shing Foundation and the 100 Talent Program of the Chinese Academy of Sciences (to GM).
Inflammasomes are multi-protein complexes that trigger the activation of caspase-1 and the maturation of interleukin-1β (IL-1β), yet the regulation of these complexes remains poorly characterized. Here we show tha...