| Protein Variants | Comment | Organism |
|---|---|---|
| additional information | generation of casp11-/- macrophages | Mus musculus |
| Localization | Comment | Organism | GeneOntology No. | Textmining |
|---|---|---|---|---|
| mitochondrion | - |
Mus musculus | 5739 | - |
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Mus musculus | P70343 | cf. caspase-4, EC 3.4.22.57 | - |
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| macrophage | - |
Mus musculus | - |
| additional information | CASP11 is not expressed in healthy tissue unless induced by infection or other pathologic stress | Mus musculus | - |
| Synonyms | Comment | Organism |
|---|---|---|
| CASP11 | - |
Mus musculus |
| caspase-11/caspase-4 | - |
Mus musculus |
| Organism | Comment | Expression |
|---|---|---|
| Mus musculus | CASP11 is induced by infection or other pathologic stress. Upregulation of CASP11 in cell lysates of infected wild-type as well as casp1-/- macrophages | up |
| General Information | Comment | Organism |
|---|---|---|
| malfunction | CASP11 deficiency improves clearance of intracellular MRSA in vitro and in vivo. Caspase-11 deficiency allows increased association of MRSA-containing vacuoles with mitochondria. Induction of mitochondrial superoxide by antimycin A (Ant A) improves MRSA eradication in casp11-/- cells, where mitochondria remain in the vicinity of the bacterium, while in wild-type macrophages, Ant A does not affect MRSA persistence. When mitochondrial dissociation is prevented by the actin depolymerizing agent cytochalasin D, Ant A effectively reduces MRSA numbers. Moreover, the absence of CASP11 leads to reduced cleavage of CASP1, IL-1beta, and CASP7, as well as to reduced production of CXCL1/KC. Reduced secretion of IL-1alpha and CXCL1/KC is found only in casp11-/- macrophages, not in caspase1-/- macrophages. Mitochondrial ROS (mtROS) contribute to MRSA clearance in casp11-/- macrophages | Mus musculus |
| metabolism | inhibition of the actin cytoskeleton prevents the dissociation of MRSA-containing phagosomes from mitochondria and leads to bacterial killing. Caspase-11 counteracts mitochondrial ROS-mediated clearance of Staphylococcus aureus in macrophages | Mus musculus |
| physiological function | inflammatory caspase-11/caspase-4 (CASP11) contributes to non-canonical NLRP3 inflammasome activation and subsequent inflammation. Methicillin-resistant Staphylococcus aureus (MRSA) is capable of persisting within professional phagocytes including macrophages. Caspase-11 counteracts mitochondrial ROS-mediated clearance of Staphylococcus aureus in macrophages, role for CASP11 in facilitating MRSA survival within murine macrophages and in promoting the persistence of Gram-positive bacteria, overview. MRSA actively prevents the recruitment of mitochondria to the vicinity of the vacuoles they reside in to avoid intracellular demise. This process requires CASP11 | Mus musculus |