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abbr. CASP11. This enzyme is a member of a family of evolutionarily conserved cysteine protease proteins known as caspases. Many of these enzymes are part of a proteolytic cascade that plays a central role in cell death by apoptosis. Caspase-11 has been isolated and characterized as ICH-3 [ICE and CED3 homolog-3]. Mouse Caspase-11 is considered the murine homolog of human caspase-4 (Van de Craen et al, 1997).

Caspase-11 gene expression in response to bacterial lipopolysaccharides and IFN-gamma requires NF-kappa-B and the signal transducer STAT1 (Schauvliege et al, 2002).

The inactive polypeptide precursor (zymogen) of murine caspase-11 (see also: Caspases) has been shown to physically interact with the proform of IL1-beta Convertase (Caspase-1). It is essential for the activation of Caspase-1 (Wang et al, 1998). It thus is directly involved in the maturation of IL1-beta and IL18 and therefore is an important mediator of inflammation. The caspase-11 zymogen itself appears to be activatable by cathepsin B (Schotte et al, 1998).

Transgenic knock-out mice with a disruption of the murine caspase-11 gene have been generated. Mutant mice are resistant to endotoxic shock induced by bacterial lipopolysaccharides. These mice do not produce IL1-alpha and IL1-beta after stimulation with bacterial lipopolysaccharides. Mutant embryonic fibroblasts have been found to be resistant to cell death by apoptosis induced by overexpression of IL1-beta Convertase (Wang et al, 1998). Mueller et al (2002) have reported, however, that apoptosis of Listeria monocytogenes-infected hepatocytes in vivo and in vitro are not altered by the absence of Caspase-11. Serum IL18 and IL1-beta levels in mice lacking Caspase-11 are similar to those in controls. Endotoxin challenged Caspase-11 deficient mice are deficient in the production of IFN-gamma. IL1-beta responses are normal with intravenous administration of LPS but decreased with intraperitoneal administration. Thus, there are alternative pathways that allow normal inflammatory and apoptotic responses during infection with L. monocytogenes.

Female Caspase-11 knock-out mice are born with a reduced number of oocyte-containing primordial follicles. This phenotype is likely due to failed cytokine processing known to occur in Caspase-11 mutants since neonatal female mice lacking both IL1-alpha and IL1-beta also exhibit a reduced endowment of primordial follicles. Normal oocyte endowment can be restored in Caspase-11 null female mice by simultaneous inactivation of the gene encoding the cell death executioner enzyme, caspase-2 (Morita et al, 2001)

Mouse microglial cells have been shown to undergo apoptosis upon inflammatory activation through bacterial lipopolysaccharides and IFN-gamma. Nitric oxide (NO) is the major autocrine mediator in this process and IRF1 (interferon regulatory factor-1) and Caspase-11 are the essential molecules in activation induced cell death of these cells. Inactivation of Caspase-11 renders microglial cells partially resistant to cell death by apoptosis induced by LPS and IFN-gamma. Inhibition of NO synthesis and Caspase-11 completely blocks LPS and IFN-gamma induced cytotoxicity. (Lee et al, 2001; Suk et al, 2002).

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