3.4.22.62: caspase-9
This is an abbreviated version!
For detailed information about caspase-9, go to the full flat file.
Word Map on EC 3.4.22.62
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3.4.22.62
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caspase-3
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bcl-2
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parp
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anti-apoptotic
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pro-apoptotic
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tunel
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necrosis
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apoptosis-related
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caspase-dependent
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apoptosis-inducing
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jnk
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apaf-1
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annexin
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extrinsic
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cyclin
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leukemia
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bid
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neuroprotective
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depolarization
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polyadp-ribose
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survivin
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hoechst
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z-vad-fmk
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antiproliferative
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adp-ribose
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xiap
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iodide
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deoxynucleotidyl
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mitochondria-dependent
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mitochondria-mediated
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cisplatin
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dutp
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fadd
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procaspase-3
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caspase-mediated
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pan-caspase
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fas-mediated
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trail
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fas-associated
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trail-induced
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bcl-2-associated
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apoptogenic
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pharmacology
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cdc25c
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puma
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transferase-mediated
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executioner
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factor-related
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deltapsim
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medicine
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tunel-positive
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sub-g1
- 3.4.22.62
- caspase-3
- bcl-2
- parp
-
anti-apoptotic
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pro-apoptotic
-
tunel
- necrosis
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apoptosis-related
-
caspase-dependent
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apoptosis-inducing
- jnk
- apaf-1
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annexin
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extrinsic
- cyclin
- leukemia
- bid
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neuroprotective
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depolarization
-
polyadp-ribose
- survivin
-
hoechst
- z-vad-fmk
-
antiproliferative
- adp-ribose
- xiap
- iodide
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deoxynucleotidyl
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mitochondria-dependent
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mitochondria-mediated
- cisplatin
- dutp
- fadd
- procaspase-3
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caspase-mediated
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pan-caspase
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fas-mediated
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trail
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fas-associated
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trail-induced
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bcl-2-associated
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apoptogenic
- pharmacology
- cdc25c
- puma
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transferase-mediated
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executioner
-
factor-related
-
deltapsim
- medicine
-
tunel-positive
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sub-g1
Reaction
strict requirement for an Asp residue at position P1 and with a marked preference for His at position P2. It has a preferred cleavage sequence of Leu-Gly-His-Asp-/-Xaa =
Synonyms
APAF, Apaf-3, apoptotic protease activating factor 3, apoptotic protease Mch-6, C14.010, CASP-9, casp9, casp9-gamma, caspase 9, caspase-9, ICE-LAP6, ICE-like apoptotic protease 6, Mch6
ECTree
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Natural Substrates Products
Natural Substrates Products on EC 3.4.22.62 - caspase-9
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REACTION DIAGRAM
inactive procaspase-7 variant C186A + H2O
active caspase-7 variant C186A + ?
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?
pro-caspase-2L + H2O
caspase-2L + ?
mechanisms of apoptotic pathways controlling fragmentation of unfertilized ovulated oocyte, caspase-3 and caspase-2L (long isoform) transcripts and proteins present in oocytes during ealy stages of meiosis, zymogen and cleaved forms
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?
pro-caspase-7 + H2O
caspase-7 + ?
mechanisms of cordycepin-induced apoptosis, activation of caspase-9, caspase-3 and caspase-7
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?
pro-caspase-9 + H2O
caspase-9
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modification at Ser196 results in alterations of proteolytic cleavage of procaspase-9 and caspase-9 activity
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?
pro-caspase-9 + H2O
caspase-9 + ?
auto-processing, apoptosis induced by tumor necrosis factor (TNF)-alpha promotes dephosphorylation of caspase-9 by casein kinase 2 (CK2), phosphorylation by casein kinase 2 decreases susceptibility of caspase-9 to cleavage by active caspase-8
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?
retinoblastoma protein Rb + H2O
p76Rb + ?
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caspase-9 interferes, upstream of the mitochondrion, with P53-induced apoptosis in both immortalized and primary fibroblasts. The involvement of caspase-9 in a premitochondrial protective pathway results from the cleavage of retinoblastoma protein Rb (tumor suppressor), at a LExD site, into a p76Rb form, which antagonizes p53-induced apoptosis
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?
?
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in P-815 cells, histamine synthesis is augmented through the post-translational cleavage of L-histidine decarboxylase, which is mediated by caspase-9
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?
L-histidine decarboxylase precursor + H2O
?
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in P-815 cells, histamine synthesis is augmented through the post-translational cleavage of L-histidine decarboxylase, which is mediated by caspase-9
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?
?
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activated caspase-9 cleaves and activates caspase-3
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?
pro-caspase-3 + H2O
caspase-3 + ?
caspase-9/-3 activation in differentiated cells can be prevented by protein kinase C (PKC) and the mitogen activated protein kinase (MEK) signaling pathways
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?
pro-caspase-3 + H2O
caspase-3 + ?
high linear energy transfer (LET) radiation enhances apoptosis by activation of caspase-3 through caspase-9
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?
pro-caspase-3 + H2O
caspase-3 + ?
induction of oxidative cell death by marine sponge extracts of Polymastia janeirensis mediated through caspase-9 apoptotic pathway
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?
pro-caspase-3 + H2O
caspase-3 + ?
mechanisms of adenosine-induced apoptosis in human colonic cancer cells
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?
pro-caspase-3 + H2O
caspase-3 + ?
mechanisms of apoptosis induced by ionizing radiation on cell lines with a different status of p53 (TP53 tumor suppressor gene), extrinsic (caspase-8 dependent) and intrinsic (caspase-9 dependent) pathways activated
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?
pro-caspase-3 + H2O
caspase-3 + ?
signalling pathways of CD20-induced apoptosis analyzed by using the chimeric mouse-human anti-CD20 antibody rituximab, activation of caspase-9 essential for rituximab-mediated apoptosis, mitochondrial role in rituximab-induced apoptosis, overexpression of caspase-9 inhibits the rituximab-induced activation of caspase-3
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pro-caspase-3 + H2O
caspase-3 + ?
mechanisms of apoptotic pathways controlling fragmentation of unfertilized ovulated oocyte, caspase-9, caspase-3 and caspase-2L (long isoform) transcripts and proteins present in oocytes during ealy stages of meiosis, zymogen and cleaved forms
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?
pro-caspase-3 + H2O
caspase-3 + ?
mechanisms of cordycepin-induced apoptosis, activation of caspase-9, caspase-3 and caspase-7
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?
pro-caspase-3 + H2O
caspase-3 + ?
requirement of caspase-3 for cell differentiation, activation of caspase-3 by caspase-9 promotes differentiation of skeletal myoblasts into myotubes
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?
pro-caspase-3 + H2O
caspase-3 + ?
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modification at Ser196 results in alterations of proteolytic cleavage of procaspase-9 and caspase-9 activity
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?
?
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endothelial cell apoptosis induced by bacteria-activated platelets requires caspase-8 and -9 and generation of reactive oxygen species
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?
additional information
?
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caspase-9 is possibly involved in the apoptotic cell death in batch and fed-batch cultures of CHO cells
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?
additional information
?
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a peroxisome proliferator-activated receptor-gamma agonist, troglitazone, facilitates caspase-8 and -9 activities by increasing the enzymatic activity of protein-tyrosine phosphatase-1B on human glioma cells
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additional information
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caspase-9 is involved in endoplasmic reticulum stress-induced apoptosis
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additional information
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caspase-9 plays a crucial role in the initiation of the initiation phase of the intrinsic apoptosis pathway. Caspase-9 gene mutation may not contribute to the pathogenesis of human cancer (gastric, colorectal and lung carcinomas)
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additional information
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caspase-9 signaling cascade induces feedback disruption of the mitochondrion during apoptosis through cleavage of anti-apoptotic Bcl-2, Bcl-xL, and Mcl-1
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additional information
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acetylserotonin-O-methyltransferase-like protein identified as a candidate substrate of caspase-9, cytoskeletal proteins associated with un-processed caspase-9 are potential candidates for structural stabilization or as caspase substrates during apoptosis
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additional information
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knockdown of the cellular-FLICE inhibitory protein (c-FLIP) using small interfering RNA (siRNA) triggers ligand-independent caspase-9-dependent spontaneous apoptosis
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additional information
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mechanisms of caspase-9 activation mediated by reactive oxygen species (ROS), caspase-9 activation facilitated by cellular oxidative state
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additional information
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threshold for the activation of caspase-9 through basal inhibitory phosphorylation at Thr125, catalyzed by the protein kinase DYRK1A
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?
additional information
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threshold for the activation of caspase-9 through basal inhibitory phosphorylation at Thr125, catalyzed by the protein kinase DYRK1A
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additional information
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the linker between the large and small subunits contains the caspase-9 auto-cleavage site (D315). Cleavage at this site generates the p35/p12 form of caspase-9. The p35/p12 form can be further processed by caspase-3 by cleavage at site D330, generating caspase-9
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additional information
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caspase-2, -3, -8 and -9 are expressed and active in the rhesus monkey corpus luteum throughout the luteal phase of the natural menstrual cycle. The primary luteotropic hormone of corpus luteum can enhance the activity of effector caspases (-2, -8, and -9) after 3-day exposure
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additional information
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caspase-2, -3, -8 and -9 are expressed and active in the rhesus monkey corpus luteum throughout the luteal phase of the natural menstrual cycle. The primary luteotropic hormone of corpus luteum, can enhance the activity of effector caspases (-2, -8, and -9) after 3-day exposure
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additional information
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activated caspase-9 prevents the accessibility of cytochrome c to complex III, resulting in the production of reactive oxygen species, and that effector caspases may depolarize mitochondria to terminate ROS production and preserve an apoptotic phenotype
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additional information
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although Apaf-1 and caspase-9 are essential for mast cell apoptosis, neither is required for the functional or clonogenic death of the cells, which may be due to mitochondrial dysfunction
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additional information
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caspase-9 is dispensable for activation of cyclin-dependent kinase 5 during cell death
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additional information
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detection of both caspase-8 and caspase-9 activity in oocytes shows that unfertilized oocytes have the machinery to undergo apoptosis by using either the extrinsic (caspase-8 dependent) or intrinsic (caspase-9 dependent) pathways
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additional information
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differential caspase-9-dependent signaling pathway between tumor necrosis factor receptor- and Fas-mediated hepatocyte apoptosis
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?
additional information
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local apoptosis of lymphatic tissue in polymicrobial sepsis is processed dependent on caspase-9
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additional information
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caspase-8-cleaved caspase-9 induces lysosomal membrane permeabilization but fails to activate the effector caspases whereas apoptosome-dependent activation of caspase-9 can trigger both events. Caspase-9 plays a dual role in cell death signaling, as an activator of effector caspases and lysosomal membrane permeabilization
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additional information
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mitochondria-dependent caspase activation for mediation of isorhamnetin-induced apoptosis
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additional information
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phosphorylation of caspase-9 at Thr125 by the protein kinase DYRK1A inhibits its cleavage and activation
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additional information
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phosphorylation of caspase-9 at Thr125 by the protein kinase DYRK1A inhibits its cleavage and activation
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additional information
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caspase-9 plays a marginal role in serum starvation-induced apoptosis. Caspase-9 sequestration represents a cellular mechanism to impair apoptosome assembly
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additional information
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caspase-9 plays a marginal role in serum starcvation-induced apoptosis. caspase-9 sequestration represents a cellular mechanism to impair apoptosome assembly
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additional information
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effect of fluoride treatment (NaF) on osteoblast proliferation, apoptosis and expression of caspase-9 mRNA in vitro
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additional information
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NO generated during hypoxia leads to activation of caspase-9 and results in initiation of caspase-cascade-dependent hypoxic neuronal death
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additional information
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activation of caspase-9 is a key step for execution of the maternally preset program of apoptosis shortly after midblastula transition in Xenopus early embryos
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