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Literature summary for 3.4.22.64 extracted from

  • Vigano, E.; Mortellaro, A.
    Caspase-11: the driving factor for noncanonical inflammasomes (2013), Eur. J. Immunol., 43, 2240-2245.
    View publication on PubMed
Search for more literature for 3.4.22.64

Protein Variants

Protein Variants Comment Organism
additional information all Casp1-/- mouse strains generated from 129 embryonic stem cells also lack caspase-11 due to a 5-bp deletion in the caspase-11 locus that causes loss of the catalytic domain. As the caspase-11 and caspase-1 loci are located physically close together, the mutations do not segregate during backcrossing, leading to double mutant mice Mus musculus

Localization

Localization Comment Organism GeneOntology No. Textmining
cytosol
-
 Mus musculus 5829
-
cytosol
-
 Homo sapiens 5829
-

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-
Mus musculus
-
-
-

Posttranslational Modification

Posttranslational Modification Comment Organism
proteolytic modification TRIF is required for the processing of procaspase-11 into the cleaved caspase-11 forms Homo sapiens
proteolytic modification TRIF is required for the processing of procaspase-11 into the cleaved caspase-11 forms. IFNs or lipopolyaccharides alone are not sufficient to trigger caspase-11 processing, but an unidentified factor derived from live Gram-negative bacteria is required, which is likely a mechanism to ensure that inflammatory responses do not proceed in the absence of active infection Mus musculus

Source Tissue

Source Tissue Comment Organism Textmining
macrophage
-
 Mus musculus
-
macrophage
-
 Homo sapiens
-

Synonyms

Synonyms Comment Organism
Ich-3
-
 Mus musculus

Expression

Organism Comment Expression
Mus musculus induction of procaspase-11 expression is delayed in Myd88-/- macrophages infected with DELTAFlag Salmonella typhimurium, although procaspase-11 processing itself remains intact additional information

General Information

General Information Comment Organism
malfunction defects in the IFN-alpha/beta, but not IFN-gamma, pathways render macrophages severely impaired in processing of caspase-11 following infection with Salmonella typhimurium, EHEC or Citrobacter rodentium, while exogenous IFN-beta rescues caspase-11 processing in Trif-/- macrophages. The absence of the TRIF-IFNAR pathway abolishes both the expression and activation of caspase-11, and treatment of Trif-/- macrophages with IFN-beta or IFN-gamma restores both the precursor and cleaved forms of caspase-11 Mus musculus
physiological function mechanisms and implications of caspase-11-mediated noncanonical inflammasome activation, importance of this pathway in regulating host defense against intracellular bacterial pathogens. The pathway engages caspase-11 to trigger both caspase-1-dependent and -independent production of the inflammatory cytokines IL-1beta, IL-18, and IL-1alpha, as well as to promote pyroptosis, a form of genetically programmed cell death that is associated with the release of such cytokines. Caspase-11 is regulated in response to extracellular stimuli, such as lipopolysaccharide and interferons Homo sapiens
physiological function mechanisms and implications of caspase-11-mediated noncanonical inflammasome activation, importance of this pathway in regulating host defense against intracellular bacterial pathogens. The pathway engages caspase-11 to trigger both caspase-1-dependent and -independent production of the inflammatory cytokines IL-1beta, IL-18, and IL-1alpha, as well as to promote pyroptosis, a form of genetically programmed cell death that is associated with the release of such cytokines. Caspase-11 is regulated in response to extracellular stimuli, such as lipopolysaccharide and interferons. Regulation of caspase-11 expression, models of activation, and caspase-11 effector functions, overview. Role of caspase-11 in pyroptosis, caspase-11 directly controls the activation of the effector caspases 3 and 7 of the apoptotic pathway independent of caspase-1 Mus musculus