The inflammasome: a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta.
By Fabio Martinon, K. Burns, J. Tschopp. Molecules and Cells, 2002
5,931 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/020f8fd4c7d1519025e367632d436091d6fcf8f8
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In Immunology
In Molecular Biology
Citations in the corpus
- Activation of the NALP3 inflammasome is triggered by low intracellular potassium concentration (2007, methodology): “To investigate the mechanism by which low intracellular potassium activates the inflammasome, we employed the in vitro inflammasome activation assay previously described by our group.(4) THP1 cells lysed in a buffer containing 10 mM KCl triggers spontaneous inflammasome assembly and caspase-1 activa”
- Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, neutral): “This inflammasome is composed of the adaptor ASC (apoptosis-associated speck-like protein containing a CARD), pro-caspase-1, and an NLR family member, such as Ipaf (Ice protease-activating factor), NALP (NAcht LRR protein) 1, or NALP3/Cryopyrin (226, 231).”
- The cell biology of inflammasomes: Mechanisms of inflammasome activation and regulation (2016, background): “NLRP1 NLRP1 was the first cytosolic receptor identified for its ability to form a caspase-1 activating platform (Martinon et al., 2002).”
- Suppression of interleukin-33 bioactivity through proteolysis by apoptotic caspases. (2009, methodology): “Proteolysis of IL-33 in Apoptotic Cell-Free Extracts To explore IL-33 processing further, we used a cell-free system based upon cytosolic extracts derived from LPS-treated monocytic THP-1 cells, where caspase-1, -4, and -5 can be activated by incubating these extracts at 37 C (Yamin et al., 1996; Ma”
- The role of glia in the spinal cord in neuropathic and inflammatory pain. (2015, background): “Rather, IL-1β is synthesised as a larger precursor protein and is cleaved into a mature form; the mechanism behind this has now been elucidated and involves caspase-1, which cleaves IL-1β, and a series of accessory proteins that form a complex known as the inflammasome that provides a platform for t”