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The inflammasome: a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta.
TLDR
It is shown that proinflammatory caspase activation and proIL-1beta processing is lost upon prior immunodepletion of Pycard, and the inflammasome constitutes an important arm of the innate immunity.
Gout-associated uric acid crystals activate the NALP3 inflammasome
TLDR
It is shown that MSU and CPPD engage the caspase-1-activating NALP3 (also called cryopyrin) inflammasome, resulting in the production of active interleukin (IL)-1β and IL-18 in mice deficient in the IL-1β receptor.
Induction of TNF Receptor I-Mediated Apoptosis via Two Sequential Signaling Complexes
TLDR
TNFR1-mediated-signal transduction includes a checkpoint, resulting in cell death (via complex II) in instances where the initial signal fails to be activated, and the cell survives.
Inhibition of death receptor signals by cellular FLIP
TLDR
The characterization of an inhibitor of apoptosis is reported, designated FLIP (for FLICE-inhibitory protein), which is predominantly expressed in muscle and lymphoid tissues and may be implicated in tissue homeostasis as an important regulator of apoptotic regulation.
The inflammasomes: guardians of the body.
TLDR
The role of NLRs, and in particular the inflammasomes, in the recognition of microbial and danger components and the role they play in health and disease are discussed.
The Inflammasomes
TLDR
Mechanisms directing normal inflammasome function and its dysregulation in disease are reviewed and emerging links between the inflammaome and pyroptosis and autophagy are examined.
Cardif is an adaptor protein in the RIG-I antiviral pathway and is targeted by hepatitis C virus
TLDR
Cardif is described, a new CARD-containing adaptor protein that interacts with RIG-I and recruits IKKα, IKKβ and IKKɛ kinases by means of its C-terminal region, leading to the activation of NF-κB and IRF3.
Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica
TLDR
It is shown that asbestos and silica are sensed by the Nalp3 inflammasome, whose subsequent activation leads to interleukin-1β secretion, and support its role as a major proinflammatory “danger” receptor in particulate matter–related pulmonary diseases.
Thioredoxin-interacting protein links oxidative stress to inflammasome activation
TLDR
The participation of TXNIP in the NLRP3 inflammasome activation may provide a mechanistic link to the observed involvement of IL-1β in the pathogenesis of type 2 diabetes.
A role for mitochondria in NLRP3 inflammasome activation
This corrects the article DOI: 10.1038/nature09663
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