EC Number   |
Substrates |
Products  |
Reversibility |
|---|
   3.4.22.64 | more |
overexpression induces apoptosis |
? |
- |
? |
| 3.4.22.64 | more |
phenotype of animals deficient in caspase-11: resistant to lipopolysaccharide-induced caspase-1 processing, interleukin-1alpha and interleukin-beta secretion, and endotoxic shock |
? |
- |
? |
| 3.4.22.64 | more |
the enzyme is a critical initiator caspase responsible for the activation of caspase-3. The enzyme is an upstream activator of caspase-1. Caspase-11 deficient animals have a reduced number of apoptotic cells and a defect in caspase-3 activation after middle cerebral artery occlusion. The enzyme is A VERY IMPORTANT REGULATOR OF APOPTOSIS |
? |
- |
? |
| 3.4.22.64 | more |
enzyme is involved in cytokine activation |
? |
- |
? |
| 3.4.22.64 | more |
pro-caspase-11 physically interacts with pro-ICE in cells, the expression of casp-11 is essential for activation of ICE. Caspase-11 is a compinent of ICE complex and is required for the activation of ICE. Important role of ICE and caspase-11 in mediating apoptosis in pathological conditions |
? |
- |
? |
| 3.4.22.64 | more |
the enzyme may play a very important role in apoptosis and inflammatory responses and may be an upstream regulator of ICE |
? |
- |
? |
| 3.4.22.64 | more |
the enzyme is involved in cytokine activation |
? |
- |
? |
| 3.4.22.64 | more |
neurotoxic effects of lipopolysaccharide on nigral dopaminergic neurons are mediated by microglial activation, interleukin-1beta, and expression of caspase-11 in mice |
? |
- |
? |
| 3.4.22.64 | more |
C/EBP homologous protein (CHOP) is crucial for the induction of caspase-11 and the pathogenesis of lipopolysaccharide-induced inflammation |
? |
- |
? |
| 3.4.22.64 | more |
neurotoxicity of 1-methyl-4-pheny-1,2,3,6-tetrahydropyridine may be mediated via activation of the caspase-11 cascade and inflammatory cascade, as well as the mitochondrial apoptotic cascade |
? |
- |
? |
