3.4.22.64: caspase-11
This is an abbreviated version!
For detailed information about caspase-11, go to the full flat file.
Word Map on EC 3.4.22.64
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3.4.22.64
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inflammasome
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pyroptosis
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lps
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lipopolysaccharide
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non-canonical
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gasdermin
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sepsis
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gsdmd
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interleukin-1
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lps-induced
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pyrin
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casp11
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apoptosis-associated
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nod-like
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caspase-5
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pore-forming
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speck-like
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guanylate-binding
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inflammasome-mediated
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wedelolactone
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rodentium
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pyroptosis-related
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inflammasome-dependent
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caspase-1/11
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caspase-1-mediated
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bmdms
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speck
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thailandensis
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medicine
- 3.4.22.64
- inflammasome
-
pyroptosis
- lps
- lipopolysaccharide
-
non-canonical
-
gasdermin
- sepsis
-
gsdmd
- interleukin-1
-
lps-induced
- pyrin
-
casp11
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apoptosis-associated
-
nod-like
- caspase-5
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pore-forming
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speck-like
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guanylate-binding
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inflammasome-mediated
- wedelolactone
- rodentium
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pyroptosis-related
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inflammasome-dependent
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caspase-1/11
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caspase-1-mediated
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bmdms
-
speck
- thailandensis
- medicine
Reaction
strict requirement for Asp at the P1 position and has a preferred cleavage sequence of (Ile/Leu/Val/Phe)-Gly-His-Asp-/- =
Synonyms
C14.012, CASP4, caspase 11, caspase-11, caspase-4, Ich-3, ICH-3 protease
ECTree
3.4.22.64 caspase-11Advanced search results
results (
results (Substrates Products
Substrates Products on EC 3.4.22.64 - caspase-11
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SUBSTRATE 
PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
Reversibility
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
acetyl-VEHD-7-amido-4-methylcoumarin + H2O
acetyl-VEHD + 7-amino-4-methylcoumarin
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cationic channel subunit transient receptor potential channel 1 + H2O
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cationic channel subunit transient receptor potential channel 1 + H2O
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i.e. TRPC1, plays a role in regulating innate immunity by modulating channel complexes during inflammatory responses
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cationic channel subunit transient receptor potential channel 1 + H2O
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cationic channel subunit transient receptor potential channel 1 + H2O
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i.e. TRPC1, plays a role in regulating innate immunity by modulating channel complexes during inflammatory responses
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procaspase-3 + H2O
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the enzyme is a critical initiator caspase responsible for the activation of caspase-3
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additional information
?
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optimal cleavage site is IEHD, LEHD, VEHD or PEHD
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additional information
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phenotype of animals deficient in caspase-11: resistant to lipopolysaccharide-induced caspase-1 processing, interleukin-1alpha and interleukin-beta secretion, and endotoxic shock
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additional information
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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
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additional information
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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
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additional information
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the enzyme may play a very important role in apoptosis and inflammatory responses and may be an upstream regulator of ICE
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additional information
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the enzyme may play a very important role in apoptosis and inflammatory responses and may be an upstream regulator of ICE
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additional information
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the enzyme is involved in cytokine activation
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additional information
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C/EBP homologous protein (CHOP) is crucial for the induction of caspase-11 and the pathogenesis of lipopolysaccharide-induced inflammation
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additional information
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caspase-11 has a regulatory role in ethanol-induced apoptosis. Suppression of caspase-11 expression may be a mechanism by which Scutellariae radix (Chinese herbal medicine) exerts its cytoprotective effect
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additional information
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neurotoxic effects of lipopolysaccharide on nigral dopaminergic neurons are mediated by microglial activation, interleukin-1beta, and expression of caspase-11 in mice
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additional information
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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
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additional information
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a pathway modulating inflammatory-cell migration involve caspase-11 and actin interacting protein 1
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additional information
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caspase-11 may be a central regulator of multiple events, including cell migration, cytokine maturation and apoptosis, during inflammation responses. Caspase-11 interacts physically and functionally with actin interacting protein 1, an activator of cofilin-mediated actin depolymerization. Caspase-11 and actin interacting protein 1 work cooperatively to promote cofilin-mediated actin depolymerization
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additional information
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Flightless-I regulates the subcellular distribution of caspase-11 by promoting its localization at the cell leading edge
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additional information
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other caspases are substrates of caspase-11
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additional information
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the enzyme may play a very important role in apoptosis and inflammatory responses and may be an upstream regulator of ICE
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additional information
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caspase-11 plays a crucial role in both inflammation and apoptosis. Caspase-11 not only activates caspase-1, that is required for the maturation of proinflammatory cytokines such as interleukin (IL)-1 and IL-18, but also activates caspase-3, leading to cellular apoptosis under pathological conditions. The expression of caspase-11 is strongly induced at both mRNA and protein levels by inflammatory stimuli such as lipopolysaccharide, interferon-Q Q, and tumor necrosis factor-K K in C6 rat glial cells as well as primary astrocytes. Induction of caspase-11 by LPS in astrocytes is mediated through the p38 MAPK pathway. Inflammatory induction of caspase-11 in astrocytes may play an important role in both inflammatory responses involving these cells and auto-regulatory apoptosis of activated astrocytes in inflammatory sites
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