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Literature summary for 3.4.22.64 extracted from

  • Stowe, I.; Lee, B.; Kayagaki, N.
    Caspase-11: arming the guards against bacterial infection (2015), Immunol. Rev., 265, 75-84.
    View publication on PubMed
Search for more literature for 3.4.22.64

Activating Compound

Activating Compound Comment Organism Structure
additional information Bacterial infection triggers caspase-11 activation , and intracellular lipopolysaccharide triggers caspase-11 activation, Toll-like receptor 4 is dispensable for caspase-11 triggering by cytoplasmic lipopolysaccharide, mechanism, detailed overview Mus musculus

Protein Variants

Protein Variants Comment Organism
additional information generation of Casp11-/- knockout mice, overview. The common mouse knockout strategy is to inject genetically targeted 129-derived ES cells into host C57BL/6 blastocysts and then backcross the chimera with other strains, commonly C57BL/6, for over 10 generations Mus musculus

Localization

Localization Comment Organism GeneOntology No. Textmining
cytosol
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 Mus musculus 5829
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Organism

Organism UniProt Comment Textmining
Mus musculus
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-
-

Source Tissue

Source Tissue Comment Organism Textmining
epithelial cell
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 Mus musculus
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macrophage
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 Mus musculus
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General Information

General Information Comment Organism
evolution inflammatory caspases all share a similar prodomain at the N-terminus responsible for protein-protein interactions: the caspase activation and recruitment domain (CARD). The genes of the inflammatory caspases are all located adjacent to the Casp1 gene on the mammalian chromosome (chromosome 9 in mouse), forming an inflammatory gene cluster. The close proximity of these genes and the high degree of similarity in the caspase protein structures might explain that the multiple inflammatory caspases arose from amplification of the Casp1 gene locus in the early stages of mammalian evolution Mus musculus
malfunction Casp11-/- knockout mouse strains are resistant to developing lethal sepsis Mus musculus
metabolism Gram-negative bacteria are specifically detected via a surveillance mechanism that involves activation of extracellular receptors such as Toll-like receptors followed by intracellular recognition and activation of pathways such as caspase-11. Extracellular LPS primarily stimulates TLR4, which can serve as a priming signal for expression of inflammasome components. Intracellular LPS can then trigger caspase-11-dependent inflammasome activation in the cytoplasm. Bacterial infection triggers caspase-11 activation and leads to two distinct signals: (i) caspase-1-dependent interleukin-1beta/interleukin-18 secretion and caspase-1-independent pyroptosis Mus musculus
physiological function caspase-11 plays a role in the inflammasome in the cytoplasm. Activation of inflammatory caspases, e.g. caspase-11, leads to the processing and maturation of inflammatory cytokines, such as interleukin-1beta and interleukin-18, as well as a specific form of cell death termed pyroptosis. Caspase-11 can induce cell death and form hetero-complexes with caspase-1. Caspase-11 by itself inefficiently cleaves pro-interleukin-1beta, suggesting early on that caspase-11 might rely on caspase-1 for cytokine maturation. The caspase-11 non-canonical inflammasome plays a significant role in Gram-negative bacterial infections, including Escherichia coli, Citrobacter rodentium, Shigella flexneri, Salmonella typhimurium, Legionella pneumophila, and Burkholderia thailandensis, caspase-11 can restrict the replication of intracellular pathogenic bacteria (Salmonella typhimurium and Burkholderia species) Mus musculus