3.4.22.36: caspase-1
This is an abbreviated version!
For detailed information about caspase-1, go to the full flat file.
Word Map on EC 3.4.22.36
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3.4.22.36
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inflammasome
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pyroptosis
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pyrin
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caspases
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nod-like
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lps
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necrosis
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tnf
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apoptosis-associated
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speck-like
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lipopolysaccharide
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adaptor
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pro-il-1
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toll-like
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card
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domain-containing
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nucleotide-binding
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neuroinflammation
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autoinflammatory
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lps-induced
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bcl-2
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domain-like
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thp-1
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multiprotein
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tunel
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microglia
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gasdermin
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danger
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marrow-derived
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interleukin-18
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leucine-rich
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cpp32
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urate
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nod2
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damage-associated
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nigericin
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medicine
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txnip
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il-1ra
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bmdms
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pan-caspase
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hmgb1
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gouty
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lymphopoietin
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monosodium
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fas-mediated
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z-vad-fmk
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fas-associated
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caspase-3-like
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pathogen-associated
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z-devd-fmk
- 3.4.22.36
- inflammasome
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pyroptosis
- pyrin
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caspases
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nod-like
- lps
- necrosis
- tnf
-
apoptosis-associated
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speck-like
- lipopolysaccharide
- adaptor
-
pro-il-1
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toll-like
-
card
-
domain-containing
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nucleotide-binding
-
neuroinflammation
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autoinflammatory
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lps-induced
- bcl-2
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domain-like
- thp-1
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multiprotein
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tunel
- microglia
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gasdermin
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danger
-
marrow-derived
- interleukin-18
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leucine-rich
- cpp32
- urate
- nod2
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damage-associated
- nigericin
- medicine
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txnip
-
il-1ra
-
bmdms
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pan-caspase
- hmgb1
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gouty
- lymphopoietin
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monosodium
-
fas-mediated
- z-vad-fmk
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fas-associated
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caspase-3-like
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pathogen-associated
- z-devd-fmk
Reaction
Strict requirement for an Asp residue at position P1 and has a preferred cleavage sequence of Tyr-Val-Ala-Asp-/- =
Synonyms
apoptosis-related cysteine protease, C14.001, CASP-1, Casp1, caspase 1, caspase-1, Csp-1, cysteine aspartyl protease-1, effector caspase, H.a.CASP1, hearm caspase-1, ICE, IL-1 beta converting enzyme, IL-1 converting enzyme, IL-1-converting enzyme, IL-1B converting enzyme, IL-1BC, IL-1beta-converting enzyme, IL-1beta–-converting enzyme, IL1beta-converting enzyme, interleukin 1, beta, convertase, interleukin converting enzyme, interleukin-1 beta converting enzyme, interleukin-1 converting enzyme, interleukin-1-converting enzyme, interleukin-1B converting enzyme, interleukin-1beta converting enzyme, interleukin-1beta-converting enzyme, interleukin-converting enzyme, p45, procaspase-1
ECTree
3.4.22.36 caspase-1Advanced search results
results (
results (Substrates Products
Substrates Products on EC 3.4.22.36 - caspase-1
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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
4-[[4'-(dimethylamino)phenyl]azo]-benzoic acid-YVADAPV-5-[(2'-aminoethyl)-amino]naphthalenesulfonic acid + H2O
4-[[4'-(dimethylamino)phenyl]azo]-benzoic acid-YVADAPV + 5-[(2-aminoethyl)-amino]naphthalenesulfonic acid
-
-
-
?
Ac-LEHD-7-amido-4-methylcoumarin + H2O
Ac-LEHD + 7-amino-4-methylcoumarin
-
-
-
-
?
acetyl-L-Leu-L-Glu-L-His-L-Asp-7-amido-4-methylcoumarin + H2O
acetyl-L-Leu-L-Glu-L-His-L-Asp + 7-amino-4-methylcoumarin
-
-
-
-
?
acetyl-L-Trp-L-Glu-L-His-L-Asp-7-amido-4-methylcoumarin + H2O
acetyl-L-Trp-L-Glu-L-His-L-Asp + 7-amino-4-methylcoumarin
-
-
-
-
?
acetyl-YVAD-7-amido-4-methylcoumarin + H2O
acetyl-YVAD + 7-amino-4-methylcoumarin
-
-
-
?
interleukin-18 + H2O
?
-
caspase-1 is required for control of oral infection with wild-type Salmonella in mice, as well as for resistance to septic shock following systemic challenge with live attenuated Salmonella enterica serovar typhimurium. Furthermore host defense against Salmonella enterica serovar typhimurium requires both caspase-1 substrates IL-1beta and IL-18
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-
?
interleukin-1beta + H2O
?
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caspase-1 is required for control of oral infection with wild-type Salmonella in mice, as well as for resistance to septic shock following systemic challenge with live attenuated Salmonella enterica serovar typhimurium. Furthermore host defense against Salmonella enterica serovar typhimurium requires both caspase-1 substrates IL-1beta and IL-18
-
-
?
N-acetyl-Asp-Glu-Val-Asp-7-amido-4-methylcoumarin + H2O
N-acetyl-Asp-Glu-Val-Asp + 7-amino-4-methylcoumarin
-
-
-
?
N-acetyl-DEVD-7-amido-4-methylcoumarin + H2O
N-acetyl-DEVD + 7-amino-4-methylcoumarin
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preferred substrate
-
-
?
N-acetyl-IETD-7-amido-4-methylcoumarin + H2O
N-acetyl-IETD + 7-amino-4-methylcoumarin
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negligible activity
-
-
?
N-acetyl-LEHD-7-amido-4-methylcoumarin + H2O
N-acetyl-LEHD + 7-amino-4-methylcoumarin
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negligible activity
-
-
?
N-acetyl-WEHD-7-amido-4-trifluoromethylcoumarin + H2O
N-acetyl-WEHD + 7-amino-4-trifluoromethylcoumarin
-
-
-
?
p35 + H2O
100000 Da fragment + 25000 Da fragment
cleavage at Asp87
-
?
pro-caspase-7 + H2O
caspase-7 + amino-terminal procaspase-7 peptide
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consensus caspase-7 recognition sequence DEVD, caspase-1 cleaves caspase-7 at the canonical activation sites Asp23 and Asp198, D23A/D198A double caspase-7 mutant is no substrate
-
-
?
pro-interleukin-33 + H2O
mature interleukin-33 + ?
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recombinant pro-interleukin-33 is cleaved by recombinant caspase-1 in vitro
-
-
?
pro-interleukin-37 + H2O
interleukin-37 propeptide
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caspase-1 processing at position D20 activates interleukin-37
-
-
?
succinyl-YVAD-7-amido-4-methylcoumarin + H2O
succinyl-YVAD + 7-amino-4-methylcoumarin
-
-
-
-
?
acetyl-WEHD-7-amido-4-methylcoumarin + H2O
acetyl-WEHD + 7-amino-4-methylcoumarin
-
-
-
-
?
acetyl-WEHD-7-amido-4-methylcoumarin + H2O
acetyl-WEHD + 7-amino-4-methylcoumarin
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WEHD is the optimal tetrapeptide recognition motif
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-
?
MyD88 adaptor-like + H2O
?
-
NF-kappaB activation by the Toll-IL-1 receptor domain protein MyD88 adapter-like is regulated by caspase-1
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-
?
MyD88 adaptor-like + H2O
?
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caspase-1 cleaves the TLR adaptor MyD88 adaptor-like at position D198
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-
?
parkin + H2O
?
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cleavage at Asp126-Ser127. Caspase-1 and caspase-8 dependent parkin cleavage in sporadic Parkinson‘s disease may play an important role in the degenerative process by initiating a vicious circle that leads to the accumulation of toxic parkin substrates, e.g. alpha-synuclein
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-
?
pre-interleukin-18 + H2O
interleukin-18 + ?
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caspase-1 regulates key steps in inflammation and immunity, by activating the proinflammatory cytokines interleukin-1beta and IL18 or mediating apoptotic processes
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-
?
pre-interleukin-18 + H2O
interleukin-18 + ?
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virus infection by influenza A or Sendai virus induces proteolytic processing of IL-18 in human macrophages via caspase-1 and caspase-3 activation
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-
?
pre-interleukin-1beta + H2O
17000 Da fragment + 28000 Da fragment
-
-
-
?
pre-interleukin-1beta + H2O
17000 Da fragment + 28000 Da fragment
cleavage to the mature interleukin-1beta
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-
?
pre-interleukin-1beta + H2O
17000 Da fragment + 28000 Da fragment
-
-
?
pre-interleukin-1beta + H2O
17000 Da fragment + 28000 Da fragment
-
-
?
pre-interleukin-1beta + H2O
interleukin-1beta + ?
-
-
-
-
?
pre-interleukin-1beta + H2O
interleukin-1beta + ?
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caspase-1 mediated maturation and secretion of IL-1beta needs a translocation competent T3SS and flagellin, but not the type III effector proteins ExoS, ExoT and ExoY. ExoS negatively regulates the Pseudomonas aeruginosa induced IL-1beta maturation by a mechanism that is dependent on its ADP ribosyltransferase activity
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-
?
pre-interleukin-1beta + H2O
interleukin-1beta + ?
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caspase-1-dependent processing of pro-interleukin-1beta can occur in the cytosol following activation of P2X7-receptor. Structural changes preceding cell death, occurring after caspase-1 activation, promote the cellular release of interleukin-1beta
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-
?
pro-caspase-7 + H2O
caspase-7 + ?
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caspase-1-mediates activation of endogenous caspase-7
-
-
?
pro-caspase-7 + H2O
caspase-7 + ?
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caspase-1-mediates activation of endogenous caspase-7
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-
?
pro-interleukin-18 + H2O
interleukin-18 + ?
-
-
-
-
?
pro-interleukin-18 + H2O
interleukin-18 + ?
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caspase-1 serves an essential function in the initiation of inflammation by proteolytically maturing the cytokines interleukin 1beta and interleukin 18
-
-
?
pro-interleukin-18 + H2O
interleukin-18 + ?
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active caspase-1 converts inactive pro-interleukin-18 to active interleukin-18
-
-
?
pro-interleukin-18 + H2O
interleukin-18 + ?
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interleukin-18 is synthesized as a 24 kDa inactive precursor lacking a signal peptide, which is cleaved after Asp35 by caspase-1 to yield an active 8 kDa molecule
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-
?
pro-interleukin-18 + H2O
interleukin-18 + ?
-
-
-
-
?
pro-interleukin-18 + H2O
interleukin-18 + ?
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activation of caspase-1 as a key event resulting in interleukin-18 production, caspase-1 is essential for interleukin-18 production in infected macrophages
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-
?
pro-interleukin-18 + H2O
interleukin-18 + ?
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caspase-1 is essential for interleukin-1beta and interleukin-18 production in the eye in response to muramyl dipeptide. Activation of NOD2 results in IL-1beta production via a caspase-1-dependent mechanism, interleukin-1beta and caspase-1 contribute to muramyl dipeptide-induced ocular inflammation, overview
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-
?
pro-interleukin-18 + H2O
interleukin-18 + ?
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active caspase-1 converts inactive pro-interleukin-18 to active interleukin-18
-
-
?
pro-interleukin-18 + H2O
interleukin-18 + ?
-
caspase-1 is essential for interleukin-1beta and interleukin-18 production in the eye in response to muramyl dipeptide. Activation of NOD2 results in IL-1beta production via a caspase-1-dependent mechanism, interleukin-1beta and caspase-1 contribute to muramyl dipeptide-induced ocular inflammation, overview
-
-
?
pro-interleukin-18 + H2O
interleukin-18 + ?
-
active caspase-1 converts inactive pro-interleukin-18 to active interleukin-18
-
-
?
pro-interleukin-18 + H2O
mature interleukin-18 + ?
-
interleukin-18 is synthesized as inactive cytoplasmic precursor that is processed into biologically activemature form in response to various proinflammatory stimuli, including viruses, by the cysteine protease caspase-1
-
-
?
pro-interleukin-1beta + H2O
17000 Da fragment + 28000 Da fragment
-
caspase-1 regulates key steps in inflammation and immunity, by activating the proinflammatory cytokines interleukin-1beta and IL18 or mediating apoptotic processes
-
-
?
pro-interleukin-1beta + H2O
17000 Da fragment + 28000 Da fragment
-
pro-interleukin-1beta cleavage site 1 is FEAD-/-, pro-interleukin-1beta cleavage site II is YVHD-/-
-
-
?
pro-interleukin-1beta + H2O
17000 Da fragment + 28000 Da fragment
pIL-1beta is mainly processed by caspase-1, but also by caspase-3
-
?
pro-interleukin-1beta + H2O
17000 Da fragment + 28000 Da fragment
pIL-1beta is mainly processed by caspase-1, but also by caspase-3
-
?
pro-interleukin-1beta + H2O
interleukin-1beta + ?
-
-
-
-
?
pro-interleukin-1beta + H2O
interleukin-1beta + ?
-
caspase-1 activation leads to release of active interleukin-1beta from THP-1 cells, regulation, overview
-
-
?
pro-interleukin-1beta + H2O
interleukin-1beta + ?
-
caspase-1 is the enzyme responsible for the cleavage and activation of interleukin-1beta, which is a potent pro-inflammatory cytokine
-
-
?
pro-interleukin-1beta + H2O
interleukin-1beta + ?
-
caspase-1 serves an essential function in the initiation of inflammation by proteolytically maturing the cytokines interleukin 1beta and interleukin 18
-
-
?
pro-interleukin-1beta + H2O
interleukin-1beta + ?
-
active caspase-1 converts inactive 31 kDa pro-interleukin-1beta to 18 kDa active interleukin-1beta
-
-
?
pro-interleukin-1beta + H2O
interleukin-1beta + ?
-
cleavage between Asp116 and Ala117, required for activation of the cytokine
-
-
?
pro-interleukin-1beta + H2O
interleukin-1beta + ?
-
-
-
-
?
pro-interleukin-1beta + H2O
interleukin-1beta + ?
-
caspase-1 is a caspase recruitment domain, CARD-containing protease required for processing of pro-interleukin-1beta in macrophages. A NOD2-NALP1 complex mediates caspase-1-dependent IL-1beta secretion in response to Bacillus anthracis infection and muramyl dipeptide, NOD2 is a NOD-like receptor, i.e. NLR. NOD2 through its N-terminal caspase recruitment domain directly binds and activates caspase-1 to trigger interleukin-1beta processing and secretion in MDP-stimulated macrophages, whereas the C-terminal leucine-rich repeats of NOD2 prevent caspase-1 activation in nonstimulated cells
-
-
?
pro-interleukin-1beta + H2O
interleukin-1beta + ?
-
caspase-1 is essential for interleukin-1beta and interleukin-18 production in the eye in response to muramyl dipeptide. Activation of NOD2 results in IL-1beta production via a caspase-1-dependent mechanism, interleukin-1beta and caspase-1 contribute to muramyl dipeptide-induced ocular inflammation, overview
-
-
?
pro-interleukin-1beta + H2O
interleukin-1beta + ?
-
active caspase-1 converts inactive 31 kDa pro-interleukin-1beta to 18 kDa active interleukin-1beta
-
-
?
pro-interleukin-1beta + H2O
interleukin-1beta + ?
-
caspase-1 is essential for interleukin-1beta and interleukin-18 production in the eye in response to muramyl dipeptide. Activation of NOD2 results in IL-1beta production via a caspase-1-dependent mechanism, interleukin-1beta and caspase-1 contribute to muramyl dipeptide-induced ocular inflammation, overview
-
-
?
pro-interleukin-1beta + H2O
interleukin-1beta + ?
-
active caspase-1 converts inactive 31 kDa pro-interleukin-1beta to 18 kDa active interleukin-1beta
-
-
?
pro-interleukin-1beta + H2O
interleukin-1beta propeptide
-
-
-
-
?
pro-interleukin-1beta + H2O
interleukin-1beta propeptide
-
-
-
-
?
pro-interleukin-1beta + H2O
mature interleukin-1beta + ?
-
-
691461, 707154, 707323, 707393, 708128, 708251, 708272, 708722, 709056, 709153, 709224, 709359, 709953, 710377
-
-
?
pro-interleukin-1beta + H2O
mature interleukin-1beta + ?
-
HMG-CoA reductase inhibition induces interleukin-1beta release through Rac1/PI3K/protein kinase B-dependent caspase-1 activation, overview. Caspase-1 is hyperactive in mevalonate kinase deficiency leading secretion of high levels of interleukin-1beta, regulation, overview
-
-
?
pro-interleukin-1beta + H2O
mature interleukin-1beta + ?
-
-
-
-
?
pro-interleukin-1beta + H2O
mature interleukin-1beta + ?
-
interleukin-1beta is synthesized as inactive cytoplasmic precursor that is processed into biologically active mature form in response to various proinflammatory stimuli, including viruses, by the cysteine protease caspase-1
-
-
?
pro-interleukin-1beta + H2O
mature interleukin-1beta + ?
-
caspase-1 effectively cleaves interleukin-1beta to its mature form in both heat shock and 37°C conditions
-
-
?
pro-interleukin-1beta + H2O
mature interleukin-1beta + ?
-
caspase-1 effectively cleaves interleukin-1beta to its mature form in both heat shock and 37°C conditions
-
-
?
pyrin + H2O
?
-
caspase-1 cleaves pyrin at Asp330, Familial Mediterranean fever-associated mutants are cleaved more than wild-type pyrin by caspase-1. Pyrin itself regulates caspase-1 activation and interleukin-1beta production through interaction of its N-terminal PYD motif with the ASC adapterprotein, and also modulates interleukin-1beta production by interaction of its C-terminal B30.2 domain with the catalytic domains of caspase-1
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-
?
succinyl-YVAD-4-nitroanilide + H2O
succinyl-YVAD + 4-nitroaniline
-
-
-
?
additional information
?
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cell death protease essential for development. Loss of zygotic caspase-1 function in Drosophila causes larval lethality and melanotic tumors
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-
?
additional information
?
-
-
the enzyme is involved in cytokine activation
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-
?
additional information
?
-
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the production of the active enzyme induces the activation of an endogenous 32000 Da (CPP32) like caspase
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-
?
additional information
?
-
-
caspase 1 activated by protease-activating factor acts upstream of mitochondria to cause release of proteins that are known to mediate apoptosis
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-
?
additional information
?
-
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caspase-1 is an upstream positive regulator of caspase-6-mediated cell death in primary human neurons
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-
?
additional information
?
-
-
anisomycin-induced activation of preformed pro-interleukin-18 is mediated by a p38 MAPK/caspase-1-dependent mechanism, whereas anisomycin-induced new synthesis of pro-interleukin-18 mRNA is mediated through p38 MAPK-dependent but caspase-1 independent mechanism
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-
?
additional information
?
-
-
caspase-1 activation of lipid metabolic pathways in response to bacterial pore-forming toxins promotes cell survival
-
-
?
additional information
?
-
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caspase-1 is involved in ER/Golgi-independent protein secretion. Caspase-1 activation by the inflammasome is directly linked to IL-1a secretion from activated macrophages and UV-irradiated keratinocytes. Secretion of FGF-2 also depends on caspase-1 expression and activity. Both proteins bind to caspase-1, suggesting a role of the protease as a carrier in an ER/Golgi-independent protein secretion pathway. Secretion of caspase-1 itself requires enzymatic activity, and caspase-1 inhibition therefore prevents secretion of its binding proteins
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-
?
additional information
?
-
-
caspase-1 activation is mediated and regulated by inflammasomes, AIM2 recognizes cytosolic dsDNA and forms a caspase-1-activating inflammasome with ASC, i.e. apoptosis-associated speck-like protein containing a caspase activation and recruitment domain. the PYHIN, i.e. pyrin and HIN domain-containing protein acts as a receptor for cytosolic DNA, which regulates caspase-1. The HIN200 domain of AIM2 binds to DNA, whereas the pyrin domain, but not that of the other PYHIN family members, associates with the adaptor molecule ASC to activate both NF-kappaB and caspase-1. Knockdown of Aim2 abrogates caspase-1 activation in response to cytoplasmic double-stranded DNA and the double-stranded DNA vaccinia virus
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-
?
additional information
?
-
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caspase-1 is an inflammatory caspase that controls the activation and secretion of the inflammatory cytokines, interleukin-1beta and interleukin-18, active caspase-1 specifically mediates secretion of retinoic acid inducible gene-I, which is not a substrate for proteolytic cleavage by caspase-1, but caspase-1 physically interacts with full length RIG-I, although not with mutant forms lacking either the amino- or carboxyl-terminal domains
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?
additional information
?
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caspase-1 is crucial in mediating neuronal apoptosis and inflammation after mechanical trauma, upregulated caspase-1 in the hours after trauma precedes neuron loss and mRNA and protein levels of interleukin-1beta and interleukin-18 are also increased. Caspase-1 is activated and central to neuronal damage in disparate brain injuring events: neonatal exposure to high O2 levels, cold injury, ischemic injury, excitotoxic injury, acceleration injury, the neurotoxic recreational drug methylenedioxymethamphetamine, MDMA, and others
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?
additional information
?
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caspase-1 is the prototype of the inflammatory caspases and is a component of the NALP3 inflammasome, a cytosolic multiprotein complex that mediates the processing of pro-inflammatory caspases and cytokines. The inflammasome represents the first line of defense against cellular stress and is a crucial component of innate immunity. Caspase-1 plays a central role in the mechanisms leading to labor particularly in the context of intrauterine infection/inflammation. Caspase-1 is increased in the amniotic fluid of women with preterm labor in the presence of intra-amniotic infection/inflammation
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?
additional information
?
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caspase-1 promotes the maturation of proinflammatory cytokines interleukin-1beta and interleukin-18
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?
additional information
?
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inflammasomes, multiprotein complexes, regulate caspase-1-activation, requiring members of the Nod-like receptor family, including NLRP1, NLRP3 and NLRC4, and the adaptor ASC, and playing a role in regulation of immune responses and disease pathogenesis, recognition mechanisms, inflammasome regulation system, overview. Several diseases are associated with dysregulated activation of caspase-1 and secretion of interleukin-1beta. Infection of macrophages with several Gram-negative bacteria, including Salmonella typhimurium, Legionella pneumophila and Pseudomonas aeruginosa, activates caspase-1 via NLRC4 and ASC
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?
additional information
?
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mevalonate kinase deficiency patients have overactive caspase-1, causing enhanced interleukin-1beta processing and subsequent inflammation in response to bacterial components
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?
additional information
?
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Nod-like receptors induce assembling of the inflammasome multiprotein complexes to activate caspase-1 in response to microbial and danger signals, overview. Superoxide dismutase 1 regulates caspase-1 and endotoxic shock, a physiological posttranslational mechanism, overview. Redox-sensitive cysteine residues regulate caspase-1 to identify the redox-sensitive cysteine residues in caspase
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?
additional information
?
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pro-inflammatory cytokine interleukin-18 and its activator caspase-1 are involved in acute liver failure and acute-on-chronicliver-failure
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?
additional information
?
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pyrin and caspase-1 interact in their pathway for NF-kappaB activation, mechanism and regulation, overview
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?
additional information
?
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the downstream signaling pathway of TLR7 and TLR8 in monocytes and dendritic cells after stimulation with specific ligands included not only the secretion of cytokines, such as TNFalpha and interleukin-1beta, but as well the activation of necessary regulating proteins like caspase-1
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?
additional information
?
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the inflammasome is a large multiprotein complex whose assembly leads to the activation of caspase-1. Proteins encoded by the nucleotide-binding domain and leucine-rich repeat, NLR, containing gene family form the central components of inflammasomes and act as intracellular sensors to detect cytosolic microbial components and danger signals, such as ATP and toxins, detailed overview. NLRs consist of three domains, besides others an N-terminal region including protein interaction domains such as the caspase recruitment domain
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?
additional information
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caspase-1-cleaved peptides show propensity for hydrophobic residues at P4
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?
additional information
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caspase-1 and caspase-9 share 100% aspartic acid in the P1 position. The structures in the cleavage sites of most caspase-1 substrates are different from that of caspase-9 substrates in the following three aspects, 1. the amino acid residues with the statistically high frequencies 2. the hydrophobic amino acid occurrence frequencies and 3. the charged amino acid occurrence frequencies, second, the amino acid pairs P1-P1' are different
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?
additional information
?
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phenotype of aninmals deficient in caspase-1: defective lipopolysaccharide-induced secretion of interleukin-1alpha and interleukin-beta and gamma-interferon, resists endotoxic shock, thymocytes partially resistant to Fas-mediated apoptosis
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?
additional information
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the enzyme induces apoptosis in transfected cells
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?
additional information
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the enzyme induces apoptosis in transfected cells
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?
additional information
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bone marrow derived. Anthrax lethal toxin and Salmonella elicit the common cell death pathway of caspase-1-dependent pyroptosis via distinct mechanisms. Activation of caspase-1 by Bacillus anthracis lethal toxin requires binding, uptake, and endosome acidification to mediate translocation of lethal factor into the host cell cytosol. Catalytically active lethal factor cleaves cytosolic substrates and activates caspase-1 by a mechanism involving proteasome activity and potassium efflux. Lethal toxin activation of caspase-1 requires the inflammasome adapter Nalp1. Salmonella infection activates caspase-1 through an independent pathway requiring the inflammasome adapter Ipaf. These distinct mechanisms of caspase-1 activation converge on a common pathway of caspase-1-dependent cell death featuring DNA cleavage, cytokine activation, and, ultimately, cell lysis resulting from the formation of membrane pores between 1.1 and 2.4 nm in diameter and pathological ion fluxes that can be blocked by glycine
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additional information
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caspase-1 is critical for IFN-gamma-mediated control of Anaplasma phagocytophilum infection
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caspase-1 is important in the host response to sepsis at least in part via its ability to regulate sepsis-induced splenic cell apoptosis
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caspase-1 is involved in ER/Golgi-independent protein secretion. Caspase-1 activation by the inflammasome is directly linked to IL-1a secretion from activated macrophages and UV-irradiated keratinocytes. Secretion of FGF-2 also depends on caspase-1 expression and activity. Both proteins bind to caspase-1, suggesting a role of the protease as a carrier in an ER/Golgi-independent protein secretion pathway. Secretion of caspase-1 itself requires enzymatic activity, and caspase-1 inhibition therefore prevents secretion of its binding proteins
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caspase-1-mediated macrophage necrosis is the source of the cytokine storm and rapid disease progression in anthrax lethal toxin-treated BALB/c mice
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functional role for caspase-1-mediated myocardial apoptosis contributing to the progression of heart failure
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IRF-2 acts as a transcriptional repressor of Casp1. Absence of IRF-2 renders macrophages more sensitive to apoptotic stimuli in a caspase-1-dependent process
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caspase-1 activation contributes to the development of nitrogen-containing bisphosphonate-associated inflammatory side effects including jaw osteomyelitis, overview
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caspase-1 activation dependent on Nalp1b, an inflammasome component, mediates cell death after pathogen infection, e.g. of dendritic cells after infection by Bacillus anthracis and lethal anthrax toxin, overview. Some dendritic cells of a certain genotype follow a caspase-1-independent way of response to infection by Bacillus anthracis, overview
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caspase-1 activation induced by MDP and ATP requires pore-forming pannexin-1, for delivery of the inducer MDP into the cell, and cryopyrin but is independent of Nod2
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caspase-1 activation is a key feature of the innate immune response of macrophages elicited by pathogens and a variety of toxins
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caspase-1 activation is mediated and regulated by inflammasomes, AIM2 recognizes cytosolic dsDNA and forms a caspase-1-activating inflammasome with ASC, i.e. apoptosis-associated speck-like protein containing a caspase activation and recruitment domain. the PYHIN, i.e. pyrin and HIN domain-containing protein acts as a receptor for cytosolic DNA, which regulates caspase-1. The HIN200 domain of AIM2 binds to DNA, whereas the pyrin domain, but not that of the other PYHIN family members, associates with the adaptor molecule ASC to activate both NF-kappaB and caspase-1. Knockdown of Aim2 abrogates caspase-1 activation in response to cytoplasmic double-stranded DNA and the double-stranded DNA vaccinia virus
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caspase-1 is activated by the inflammasomes and is responsible for the proteolytic maturation of the cytokines interleukin-1beta and interleukin-18 during infection and inflammation
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caspase-1 is crucial in mediating neuronal apoptosis and inflammation after mechanical trauma, upregulated caspase-1 in the hours after trauma precedes neuron loss and mRNA and protein levels of interleukin-1beta and interleukin-18 are also increased
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caspase-1 mediates cell death and secretion of interleukin-1beta in native macrophages infected with Yersinia enterocolitica and Yersinia pestis, but cell death occurs independently of caspase-1 in Yersinia pestis strain KIM5, while translocation of catalytically active bacterial YopJ into macrophages is required for caspase-1 activation and cell death, regulation, overview
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caspase-1 mediates resistance in murine melioidosis, caused by gram-negative rod Burkholderia pseudomallei, which can induce caspase-1-dependent cell death in macrophages. Caspase-1-dependent rapid cell death might contribute to resistance by reducing the intracellular niche for Birkholderia pseudomallei, but, in addition, caspase-1 might also have a role in controlling intracellular replication of Burkholderia pseudomallei in macrophages
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caspase-1 promotes the maturation of proinflammatory cytokines interleukin-1beta and interleukin-18
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critical involvement of pneumolysin in production of interleukin-1alpha and caspase-1-dependent cytokines in infection with Streptococcus pneumoniae in vitro
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enzyme regulation, mechanisms of ATP-induced and caspase-1-dependent cell death and interleukin-1beta release are both regulated by zinc, overview
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inflammasomes, multiprotein complexes, regulate caspase-1-activation, requiring members of the Nod-like receptor family, including NLRP1, NLRP3 and NLRC4, and the adaptor ASC, and playing a role in regulation of immune responses and disease pathogenesis, recognition mechanisms, overview. Several diseases are associated with dysregulated activation of caspase-1 and secretion of interleukin-1beta
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the enzyme is involved in the cytokine metabolism, cryopyrin and caspase-1 are central to both innate immunity and to moderating lung pathology in influenza pneumonia, absence of cryopyrin and caspase-1, but not Ipaf, is associated with greater mortality, regulation, overview
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the inflammasome is a large multiprotein complex whose assembly leads to the activation of caspase-1. Proteins encoded by the nucleotide-binding domain and leucine-rich repeat, NLR, containing gene family form the central components of inflammasomes and act as intracellular sensors to detect cytosolic microbial components and danger signals, such as ATP and toxins, detailed overview. NLRs consist of three domains, besides others an N-terminal region including protein interaction domains such as the caspase recruitment domain
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the inflammasome regulatory proteins, ASC or apoptosis-associated speck-like protein containing a caspase-recruitment domain, and NLRP3 or NLR family, pyrin domain containing 3, are essential for caspase-1 activation, and also for P2X7 receptor-stimulated secretion of MHC class II-containing exosomes requires the ASC/NLRP3 inflammasome, which is, however, independent of caspase-1, overview
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peptide substrate screening, the enzyme preferably cleaves after Asp, overview
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the enzyme induces apoptosis in transfected cells
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caspase-1 activation is a key feature of the innate immune response of macrophages elicited by pathogens and a variety of toxins
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additional information
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caspase-1 activation induced by MDP and ATP requires pore-forming pannexin-1, for delivery of the inducer MDP into the cell, and cryopyrin but is independent of Nod2
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additional information
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the inflammasome regulatory proteins, ASC or apoptosis-associated speck-like protein containing a caspase-recruitment domain, and NLRP3 or NLR family, pyrin domain containing 3, are essential for caspase-1 activation, and also for P2X7 receptor-stimulated secretion of MHC class II-containing exosomes requires the ASC/NLRP3 inflammasome, which is, however, independent of caspase-1, overview
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additional information
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caspase-1 is activated by the inflammasomes and is responsible for the proteolytic maturation of the cytokines interleukin-1beta and interleukin-18 during infection and inflammation
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additional information
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peptide substrate screening, the enzyme preferably cleaves after Asp, overview
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caspase-1 is a negative regulator of AMPA receptor-mediated long-term potentiation at hippocampal synapses
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in brain microvascular endothelial cells and in astrocytes expression and activity of inducible nitric axide synthase exclusively depends on the endogenous availability of bioactive interleukin-1beta as inhibition of ICE activity significantly decreases promoter activity of inducible nitric axide synthase, expression and enzyme activity
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caspase-1 activation is mediated and regulated by inflammasomes, AIM2 recognizes cytosolic dsDNA and forms a caspase-1-activating inflammasome with ASC, i.e. apoptosis-associated speck-like protein containing a caspase activation and recruitment domain. the PYHIN, i.e. pyrin and HIN domain-containing protein acts as a receptor for cytosolic DNA, which regulates caspase-1. The HIN200 domain of AIM2 binds to DNA, whereas the pyrin domain, but not that of the other PYHIN family members, associates with the adaptor molecule ASC to activate both NF-kappaB and caspase-1. Knockdown of Aim2 abrogates caspase-1 activation in response to cytoplasmic double-stranded DNA and the double-stranded DNA vaccinia virus
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caspase-1 is crucial in mediating neuronal apoptosis and inflammation after mechanical trauma, upregulated caspase-1 in the hours after trauma precedes neuron loss and mRNA and protein levels of interleukin-1beta and interleukin-18 are also increased
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the enzyme is able to induce apoptosis in Sf9 cells
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the enzyme is able to induce apoptosis in Sf9 cells
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caspase-1 is involved in this apoptosis
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