Non-canonical inflammasome activation targets caspase-11

By N. Kayagaki, S. Warming, M. Lamkanfi, L. Walle, S. Louie, Jennifer Dong, K. Newton, Yan Qu, Jinfeng Liu, Sherry Heldens and 4 more. Nature, 2011

2,444 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/c85407eee3f2ff4e9e5ffc17cc1b72163569cacc

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Citations in the corpus

Pyroptosis in inflammatory diseases and cancer (2022, background): “Extracellular LPS can induce the expression of type I interferon, which then forms a feedback loop and activates type I interferon receptor to induce caspase-11 expression [33, 34].”
Canonical Nlrp3 inflammasome links systemic low grade inflammation to functional decline in aging (2013, positive): “Also, caspase-11 and not caspase-1 is the major sensor of LPS and regulates endotoxemia-associated lethality in mice (Kayagaki et al., 2011).”
Nek7 is an essential mediator of NLRP3 activation downstream of potassium efflux (2016, positive): “Consistent with previous studies 15–17 , cytotoxicity induced by cytosolic LPS required caspase 11, but not NLRP3 or Nek7 (Extended Data Fig.”
Human Monocytes Engage an Alternative Inflammasome Pathway. (2016, neutral): “More recently, it has become evident that lipopolysaccharide (LPS) from gram-negative bacteria is directly sensed by caspase-11 or its human orthologs caspase-4 and caspase-5 in the cytosol to trigger cell death and activate the NLRP3 inflammasome (Kayagaki et al., 2011; Shi et al., 2014).”
Caspases in cell death, inflammation and disease (2019, background): “Murine caspase-11 autonomously cleaves GSDMD to induce pyroptosis as highlighted by the observation that extracellular release of the DAMPs IL-1α and HMGB1 from macrophages infected with Escherichia coli, Citrobacter rodentium and Vibrio cholerae was fully caspase-11-dependent (Kayagaki et al., 2011”
Sepsis: current dogma and new perspectives. (2014, background): “Inhibition or deletion of pro-caspase-1, caspase-1, or PKR interferes with inflammasome signaling and confers protection against lethality in murine sepsis by inhibiting HMGB1 release without suppressing antimicrobial mechanisms (Kayagaki et al., 2011; Lamkanfi et al., 2010; Lu et al., 2012).”
Pyroptosis: Gasdermin-Mediated Programmed Necrotic Cell Death. (2017, background): “Recently, a 5-nt deletion was identified in Casp11 of strain 129 mice (which produce a truncated nonfunctional caspase-11), and it is the loss of Casp11 but not Casp1 that could protect mice from endotoxic shock [19].”