3.4.22.61: caspase-8
This is an abbreviated version!
For detailed information about caspase-8, go to the full flat file.
Word Map on EC 3.4.22.61
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3.4.22.61
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caspase-9
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bcl-2
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necrosis
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extrinsic
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bid
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tnf
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trail
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apoptosis-inducing
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parp
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pro-apoptotic
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anti-apoptotic
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leukemia
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fas-associated
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trail-induced
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tunel
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fasl
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annexin
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death-inducing
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factor-related
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caspase-dependent
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c-flips
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apoptosis-related
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xiap
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fas-mediated
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flip
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receptor-mediated
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nf-kappab
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polyadp-ribose
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jurkat
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necroptosis
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anti-fas
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deoxynucleotidyl
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adp-ribose
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pan-caspase
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z-vad-fmk
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tnf-related
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deltapsim
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mitochondria-dependent
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fas-induced
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survivin
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receptor-induced
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tnf-induced
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receptor-interacting
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mlkl
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mitochondria-mediated
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ripk1
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sub-g1
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apaf-1
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executioner
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drug development
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procaspase-3
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medicine
- 3.4.22.61
- caspase-9
- bcl-2
- necrosis
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extrinsic
- bid
- tnf
-
trail
-
apoptosis-inducing
- parp
-
pro-apoptotic
-
anti-apoptotic
- leukemia
-
fas-associated
-
trail-induced
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tunel
- fasl
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annexin
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death-inducing
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factor-related
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caspase-dependent
- c-flips
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apoptosis-related
- xiap
-
fas-mediated
- flip
-
receptor-mediated
- nf-kappab
-
polyadp-ribose
-
jurkat
-
necroptosis
-
anti-fas
-
deoxynucleotidyl
- adp-ribose
-
pan-caspase
- z-vad-fmk
-
tnf-related
-
deltapsim
-
mitochondria-dependent
-
fas-induced
- survivin
-
receptor-induced
-
tnf-induced
-
receptor-interacting
- mlkl
-
mitochondria-mediated
- ripk1
-
sub-g1
- apaf-1
-
executioner
- drug development
- procaspase-3
- medicine
Reaction
strict requirement for Asp at position P1 and has a preferred cleavage sequence of (Leu/Asp/Val)-Glu-Thr-Asp-/-(Gly/Ser/Ala) =
Synonyms
apoptotic cysteine protease, apoptotic protease Mch-5, C14.004, CAP4, Casp8, caspase 8, caspase-8, cysteine aspartic acid protease 8, cysteine aspartic acid-specific protease, cysteine protease caspase-8, FADD-homologous ICE/CED-3-like protease, FADD-like ICE, FLICE, FLICE/MACH, ICE-like apoptotic protease 5, MACH, Mch5, More, MORT1-associated CED-3 homolog
ECTree
3.4.22.61 caspase-8Advanced search results
results (
results (Activating Compound
Activating Compound on EC 3.4.22.61 - caspase-8
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ACTIVATING COMPOUND 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
IMAGE
6'-benzyloxy-4-bromo-2'-hydroxychalcone
compound displays potent cytotoxic properties against human leukaemia cells U-937, HL-60, K-562, NALM-6 and MOLT-3. Application results in significant activation of caspase-8 after 24 h of treatment
complement factor 5a
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increases caspase-8 activity and expression level of procaspase-8, and increases caspase 8 homologue FLICE-inhibitory protein, cFLIP, activation, C5a stimulation initiated cFLIP cleavage, which increased the 43 kDa active fragment, overview
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edelfosine
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i.e. 1-O-octadecyl-2-O-methyl-racglycero-3-phosphocholine, an anti-tumor drug, induces activation of procaspase-8 in T-cell leukemia, specific inhibition of caspase-8 prevents the apoptotic response triggered by edelfosine, overview. The compound induces the generation of the so-called death-inducing signaling complex, DISC, made up of Fas/CD95, FADD, and procaspase-8, in lipid rafts
Fas death domain
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FADD, activating caspase-8 via its death-effector domain, DED. FADD dimerizes on binding to Fas, a crucial event that greatly enhances both the FADD-Fas interaction and caspase-8 activation
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Fas-associated death domain protein-like interleukin-1-beta-converting enzyme-like inhibitory protein, long form
FLIP L, results in a heterodimeric enzyme
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harmol
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i.e. 1-methyl-9H-beta-carbolin-7-ol, a natural beta-carboline plant alkaloid, induces caspase-8 activation
homocysteine
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induces the enzyme activation 3.5fold in endothelial progenitor cells at 0.2 mM
lithium/SB-415286
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two GSK-3 inhibitor, enhance caspase-8 activity in hepatoma cells, but not in healthy hepatocyte, and increase the sensitivity of the cells to tumor necrosis factor-related apoptosis-inducing ligand, i.e. TRAIL, or CH-11, a CD95 agonistic antibody, which leads to increased apoptosis, the agents have no effect alone, mechanism, overview, 1.5-2.1fold activation of CH-11-induced apoptosis at 20 mM LiCl and 0.025 mM SB-415286
NPI-0052
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the chemotherapeutic agent, i.e. salinosporamide A, a proteasome inhibitor, activates the caspase-8-dependent apoptosis pathway in multiple myeloma cells, it potentiates the apoptosis induced by TNF-alpha, bortezomib, and thalidomide, regulation, overview
resveratrol
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causes activation of caspase-8, which in turn results in modulation of mitochondrial apoptotic machinery to promote apoptosis of rheumatoid arthritis fibroblast-like synoviocytes
TNF-alpha/irradiation
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leads to an increase of caspase-8 activity up to 3.2fold within 24 h and up to 4.4fold within 48 h after irradiation, administration of TNF-alpha to non-irradiated hepatocytes does not lead to an increased activity of caspase-8
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tumor necrosis factor-alpha
increases activity after 24 h exposure
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CD95
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FLICE is the first in a cascade of ICE-like proteases activated by CD95. This activation requires a functional CD95 disc
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CD95
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FLICE is the first in a cascade of ICE-like proteases activated by CD95. This activation requires a functional CD95 disc
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FLIPL protein
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a catalytically defective caspase-8 paralogue, can interact with caspase-8 to activate its catalytic function
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FLIPL protein
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a catalytically defective caspase-8 paralogue, can interact with caspase-8 to activate its catalytic function
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additional information
combination of interferon-alpha/TRAIL increases activity significantly
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additional information
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combination of interferon-alpha/TRAIL increases activity significantly
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additional information
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alpha-trifluoromethyl acyloins TF2 and TF3, i.e. CF3CH(OH)COPh and CF3CH(OH)COCH2Ph, fail to activate caspase-8 in both HSC-2 and HSC-4 cells during 4-24 hours treatment, however, TF2 and TF3 induce apoptotic cell death in human submandibular gland carcinoma cells
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additional information
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caspase-8 is activated by homodimerization, which also leads to autoproteolytic processing of the enzyme into multiple smaller species
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additional information
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caspase-8 is activated downstream of the death receptor signaling or via death receptor-independent pathway
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additional information
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CTX III, from crude venom of Naja naja atra, induces the activation of caspase-8 as part of the caspase-8-dependent Bid-Bax pathway, overview
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additional information
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engagement of Fas causes a rapid activation of caspase-8, induction of caspase-8 by Fas ligand, FasL, overview. Increased S-glutathionylation of Fas, caspase-8 activity, and cell death in cells lacking Grx1
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additional information
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Leptospira interrogans induces apoptosis in macrophages and hepatocytes via caspase-8- and caspase-3-dependent pathways
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additional information
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no enzyme activation by natural beta-carboline alkaloids harmalol, harmine, and harmaline, i.e. 1-methyl-4,9-dihydro-3H-beta-carbolin-7-ol, 7-methoxy-1-methyl-9H-beta-carboline, and 7-methoxy-1-methyl-4,9-dihydro-3H-beta-carboline, respectively
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additional information
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obatoclax enhances TRAIL-mediated apoptosis, which is accompanied by activation of caspase-8, -9, and -3 and cleavage of Bid. A feedback amplification loop mediated by caspase-3 may contribute to activation of caspase-8 and Bid, overview
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additional information
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procaspase-8 is cleaved to 41 and 43 kDA fragments for activation, overview
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additional information
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rosiglitazone, i.e. BRL, induces procaspase-8 cleavage and activation to caspase-8 leading to apoptosis in breast cancer cells. Rosiglitazone transactivates the FasL promoter gene in a peroxisome proliferator-activated receptor gamma PPARgamma-dependent manner
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additional information
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the antioxidant 7,8-diacetoxy-4-methylcoumarin, DAMC, and its thiocoumarin derivative 7,8-diacetoxy-4-methylthiocoumarin, DAMTC, induce apoptosis by activating caspase-9 and caspase-3 without affecting the activity of caspase-8
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additional information
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the interferon regulatory factor 5, IRF-5, induces caspase-8 activation
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additional information
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TNF-related apoptosis-inducing ligand and etoposide induce caspase-8 activation, which is inhibited by caspase inhibitor N-carbobenzyloxy-VAD-fluoromethyl ketone, but not by M-791
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additional information
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tumor necrosis factor-related apoptosis-inducing ligand, i.e. Apo2L/TRAIL, is a death messenger that induces apoptosis in many types of human hematological neoplasia including multiple myeloma by inducing activation of caspase-8 and caspase-3. Bortezomib enhances the activating effect on capsase-8
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additional information
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caspase-8 integration into cardiolipin-rich domains of the outer mitochondrial membrane results in full activation of this caspase which can then directly access and cleave its substrate Bid
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additional information
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tumor necrosis factor alpha stimulation results in a caspase-8-dependent Her-2 cleavage in MCF-7 breast adenocarcinoma cells defective for nuclear factor kappaB activation
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additional information
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active caspase-8 is upregulated under irradiation stress, and interleukin-1 does not prevent it when used in pretreatment, overview
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additional information
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caspase-8 expression is increased in the orbito-frontal cortex 14 days after spared nerve injury of the sciatic nerve, prevented by ozone
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additional information
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caspase-8 expression is induced by Fas, and L-carnitine induces Fas and caspase-8
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additional information
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caspase-8 is induced in brain by cerebral ischemia. Upon activation, the cytoplasmic adaptor protein Fas-associated death domain associates with the death domain of Fas, followed by recruitment and activation of caspase-8
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additional information
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Leptospira interrogans induces apoptosis in macrophages and hepatocytes via caspase-8- and caspase-3-dependent pathways
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additional information
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no induction or activation of caspase-8 by cordycepin in MA-10 mouse Leydig tumor cells, overview
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additional information
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PBOX-21/STI571 induces activation of caspase-8 leading to aopotosis
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additional information
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caspase-8 activation involves dimerization and subsequent interdomain autoprocessing of caspase-8 zymogens, mechanism, overview. The inactive caspase-8 paralogue FLIPL is able to activate caspase-8 by heterodimerization
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additional information
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irradiation induces TNF-alpha-mediated activation of caspase-8, and apoptosis in hepatocytes. Apoptosis induction is prevented by IkappaB antisense oligonucleotides mediated by suppression of caspases-9 and -3 activation but not of caspase-8 activation, overview
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