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Ac-LEDH-4-nitroanilide + H2O
Ac-LEDH + 4-nitroaniline
-
-
-
-
?
acetyl-Asp-Glu-Val-Asp-p-nitroanilide + H2O
acetyl-Asp-Glu-Val-Asp + p-nitroaniline
i.e. Ac-DEVD-pNA, caspase-9/-3 activation in differentiated cells can be prevented by protein kinase C (PKC) and the mitogen activated protein kinase (MEK) signaling pathways
-
-
?
acetyl-DEVD-7-amido-4-methylcoumarin + H2O
acetyl-DEVD + 7-amino-4-methylcoumarin
-
-
-
-
?
acetyl-DEVD-7-amido-4-trifluoromethylcoumarin + H2O
acetyl-DEVD + 7-amino-4-trifluoromethylcoumarin
acetyl-Ile-Glu-Thr-Asp-p-nitroanilide + H2O
acetyl-Ile-Glu-Thr-Asp + p-nitroaniline
-
13% of the activity with acetyl-Leu-Glu-His-Asp-p-nitroanilide
-
-
?
acetyl-LEHD-7-amido-4-trifluoromethyl coumarin + H2O
acetyl-LEHD + 7-amino-4-trifluoromethyl coumarin
acetyl-LEHD-7-amido-4-trifluoromethylcoumarin + H2O
acetyl-LEHD + 7-amino-4-trifluoromethylcoumarin
acetyl-Leu-Glu-His-Asp-p-nitroanilide + H2O
acetyl-Leu-Glu-His-Asp + p-nitroaniline
acetyl-Trp-Glu-His-Asp-p-nitroanilide + H2O
acetyl-Trp-Glu-His-Asp + p-nitroaniline
-
49% of the activity with acetyl-Leu-Glu-His-Asp-p-nitroanilide
-
-
?
acetyl-Val-Glu-Ile-Asp-p-nitroanilide + H2O
acetyl-Val-Glu-Ile-Asp + p-nitroaniline
-
19% of the activity with acetyl-Leu-Glu-His-Asp-p-nitroanilide
-
-
?
acetyl-VEHD-7-amido-4-methylcoumarin + H2O
?
-
-
-
-
?
benzyloxycarbonyl-Leu-Glu-His-Asp-7-amido-4-trifluoromethylcoumarin + H2O
?
-
-
-
-
?
benzyloxycarbonyl-Leu-Glu-His-Asp-7-amino-4-trifluoromethylcoumarin + H2O
?
-
-
-
-
?
IETD-7-amido-4-trifluoromethylcoumarin + H2O
IETD + 7-amino-4-trifluoromethylcoumarin
-
-
-
-
?
inactive Bid + H2O
active tBid + ?
inactive procaspase-7 variant C186A + H2O
active caspase-7 variant C186A + ?
-
-
-
-
?
L-histidine decarboxylase precursor + H2O
?
LEDH-4-nitroanilide + H2O
LEDH + 4-nitroaniline
-
-
-
-
?
LEHD-7-amido-4-methylcoumarin + H2O
LEHD + 7-amino-4-methylcoumarin
-
-
-
-
?
N-acetyl-LEHD-4-trifluoromethylcoumarin 7-amide + H2O
N-acetyl-LEHD + 7-amino-4-trifluoromethylcoumarin
-
-
-
-
?
N-acetyl-Leu-Glu-His-Asp-7-amido-4-fluorocoumarin + H2O
N-acetyl-Leu-Glu-His-Asp + 7-amino-4-fluorocoumarin
-
-
-
-
?
poly (ADP-ribose) polymerase + H2O
?
-
i.e. PARP
-
-
?
poly(ADP-ribose) polymerase + H2O
?
-
-
-
?
pro-caspase-2L + H2O
caspase-2L + ?
pro-caspase-3 + H2O
active caspase-3 + caspase-3 propeptide
-
-
-
-
?
pro-caspase-3 + H2O
caspase-3 + ?
pro-caspase-3 + H2O
caspase-3 + caspase-3 propeptide
-
-
-
-
?
pro-caspase-7 + H2O
caspase-7 + ?
pro-caspase-9 + H2O
caspase-9
-
modification at Ser196 results in alterations of proteolytic cleavage of procaspase-9 and caspase-9 activity
-
-
?
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
-
-
?
procaspase-3 + H2O
caspase-3 + ?
-
-
-
?
procaspase-7 + H2O
caspase-7 + ?
-
-
-
-
?
retinoblastoma protein Rb + H2O
p76Rb + ?
-
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
-
-
?
additional information
?
-
acetyl-DEVD-7-amido-4-trifluoromethylcoumarin + H2O
acetyl-DEVD + 7-amino-4-trifluoromethylcoumarin
apoptosome inhibitors analyzed, caspase-9 activity indirectly measured by caspase-3 assay
-
-
?
acetyl-DEVD-7-amido-4-trifluoromethylcoumarin + H2O
acetyl-DEVD + 7-amino-4-trifluoromethylcoumarin
-
activation of caspase-3 by caspase-9 indirectly measured by caspase-3 assay
-
-
?
acetyl-LEHD-7-amido-4-trifluoromethyl coumarin + H2O
acetyl-LEHD + 7-amino-4-trifluoromethyl coumarin
-
-
-
-
?
acetyl-LEHD-7-amido-4-trifluoromethyl coumarin + H2O
acetyl-LEHD + 7-amino-4-trifluoromethyl coumarin
-
-
-
?
acetyl-LEHD-7-amido-4-trifluoromethyl coumarin + H2O
acetyl-LEHD + 7-amino-4-trifluoromethyl coumarin
activity of caspase-9 determined after treatment of cells with 10 mg/ml recombinant Vibrio vulnificus cytolysin (rVVC) for 0.5, 1, 2, 3 and 4 h
-
-
?
acetyl-LEHD-7-amido-4-trifluoromethylcoumarin + H2O
acetyl-LEHD + 7-amino-4-trifluoromethylcoumarin
-
-
-
-
?
acetyl-LEHD-7-amido-4-trifluoromethylcoumarin + H2O
acetyl-LEHD + 7-amino-4-trifluoromethylcoumarin
-
-
-
?
acetyl-LEHD-7-amido-4-trifluoromethylcoumarin + H2O
acetyl-LEHD + 7-amino-4-trifluoromethylcoumarin
i.e. Ac-Leu-Glu-His-Asp-MCA, fluorescence assay, 50 microg cell lysate incubated with 5 microl of 1 mM substrate
-
-
?
acetyl-Leu-Glu-His-Asp-p-nitroanilide + H2O
acetyl-Leu-Glu-His-Asp + p-nitroaniline
-
-
-
-
?
acetyl-Leu-Glu-His-Asp-p-nitroanilide + H2O
acetyl-Leu-Glu-His-Asp + p-nitroaniline
i.e. Ac-LEHD-pNA, caspase-9/-3 activation in differentiated cells can be prevented by protein kinase C (PKC) and the mitogen activated protein kinase (MEK) signaling pathways
-
-
?
acetyl-Leu-Glu-His-Asp-p-nitroanilide + H2O
acetyl-Leu-Glu-His-Asp + p-nitroaniline
i.e. LEHD-pNA, caspase-9 activity determined, anti-apoptotic cell survival function of cadmium
-
-
?
acetyl-Leu-Glu-His-Asp-p-nitroanilide + H2O
acetyl-Leu-Glu-His-Asp + p-nitroaniline
i.e. Ac-LEHD-pNA, caspase-9 activity assay
-
-
?
inactive Bid + H2O
active tBid + ?
-
cleavage at amino acid 59
-
-
?
inactive Bid + H2O
active tBid + ?
-
cleavage at amino acid 59. Substrate mutants BidD98A and BidD75A are cleaved by caspase-9, mutant BidD59A is not cleaved
-
-
?
L-histidine decarboxylase precursor + H2O
?
-
-
-
-
?
L-histidine decarboxylase precursor + H2O
?
-
in P-815 cells, histamine synthesis is augmented through the post-translational cleavage of L-histidine decarboxylase, which is mediated by caspase-9
-
-
?
L-histidine decarboxylase precursor + H2O
?
-
-
-
-
?
L-histidine decarboxylase precursor + H2O
?
-
in P-815 cells, histamine synthesis is augmented through the post-translational cleavage of L-histidine decarboxylase, which is mediated by caspase-9
-
-
?
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
-
-
?
pro-caspase-2L + H2O
caspase-2L + ?
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
-
-
?
pro-caspase-3 + H2O
?
-
activated caspase-9 cleaves and activates caspase-3
-
-
?
pro-caspase-3 + H2O
?
-
-
-
-
?
pro-caspase-3 + H2O
?
-
increased activity of caspase-9 to 407% and of caspase-3 to 540% after cell treatment with atorvastatin
-
-
?
pro-caspase-3 + H2O
?
-
-
-
-
?
pro-caspase-3 + H2O
?
-
increased activity of caspase-9 to 407% and of caspase-3 to 540% after cell treatment with atorvastatin
-
-
?
pro-caspase-3 + H2O
caspase-3 + ?
-
-
-
-
?
pro-caspase-3 + H2O
caspase-3 + ?
-
-
-
?
pro-caspase-3 + H2O
caspase-3 + ?
-
-
-
-
?
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
-
-
?
pro-caspase-3 + H2O
caspase-3 + ?
high linear energy transfer (LET) radiation enhances apoptosis by activation of caspase-3 through caspase-9
-
-
?
pro-caspase-3 + H2O
caspase-3 + ?
induction of oxidative cell death by marine sponge extracts of Polymastia janeirensis mediated through caspase-9 apoptotic pathway
-
-
?
pro-caspase-3 + H2O
caspase-3 + ?
mechanisms of adenosine-induced apoptosis in human colonic cancer cells
-
-
?
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
-
-
?
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
-
-
?
pro-caspase-3 + H2O
caspase-3 + ?
apoptosome inhibitors analyzed, caspase-9 activity indirectly measured by caspase-3 assay
-
-
?
pro-caspase-3 + H2O
caspase-3 + ?
gradual increase in caspase-3 activities in cells treated with recombinant Vibrio vulnificus cytolysin (rVVC) during 0.5-3 h incubation and a slight decrease after incubation for 4 h
-
-
?
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
-
-
?
pro-caspase-3 + H2O
caspase-3 + ?
mechanisms of cordycepin-induced apoptosis, activation of caspase-9, caspase-3 and caspase-7
-
-
?
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
-
-
?
pro-caspase-3 + H2O
caspase-3 + ?
-
-
-
-
?
pro-caspase-3 + H2O
caspase-3 + ?
-
activation of caspase-3 by caspase-9 indirectly measured by caspase-3 assay
-
-
?
pro-caspase-3 + H2O
caspase-3 + ?
-
modification at Ser196 results in alterations of proteolytic cleavage of procaspase-9 and caspase-9 activity
-
-
?
pro-caspase-7 + H2O
caspase-7 + ?
-
-
-
-
?
pro-caspase-7 + H2O
caspase-7 + ?
mechanisms of cordycepin-induced apoptosis, activation of caspase-9, caspase-3 and caspase-7
-
-
?
additional information
?
-
-
endothelial cell apoptosis induced by bacteria-activated platelets requires caspase-8 and -9 and generation of reactive oxygen species
-
-
?
additional information
?
-
-
caspase-9 is possibly involved in the apoptotic cell death in batch and fed-batch cultures of CHO cells
-
-
?
additional information
?
-
-
no activity with acetyl-Asp-Glu-Val-Asp-p-nitroanilide and acetyl-Val-Asp-Val-Ala-Asp-p-nitroanilide
-
-
?
additional information
?
-
-
LEHD is the optimal tetrapeptide recognition motif
-
-
?
additional information
?
-
-
the preferred cleavage sequence is LEHD-/-
-
-
?
additional information
?
-
-
the preferred cleavage sequence is LEHD-/-
-
-
?
additional information
?
-
-
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
-
-
?
additional information
?
-
-
caspase-9 is involved in endoplasmic reticulum stress-induced apoptosis
-
-
?
additional information
?
-
-
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)
-
-
?
additional information
?
-
-
caspase-9 signaling cascade induces feedback disruption of the mitochondrion during apoptosis through cleavage of anti-apoptotic Bcl-2, Bcl-xL, and Mcl-1
-
-
?
additional information
?
-
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
-
-
?
additional information
?
-
knockdown of the cellular-FLICE inhibitory protein (c-FLIP) using small interfering RNA (siRNA) triggers ligand-independent caspase-9-dependent spontaneous apoptosis
-
-
?
additional information
?
-
mechanisms of caspase-9 activation mediated by reactive oxygen species (ROS), caspase-9 activation facilitated by cellular oxidative state
-
-
?
additional information
?
-
threshold for the activation of caspase-9 through basal inhibitory phosphorylation at Thr125, catalyzed by the protein kinase DYRK1A
-
-
?
additional information
?
-
-
threshold for the activation of caspase-9 through basal inhibitory phosphorylation at Thr125, catalyzed by the protein kinase DYRK1A
-
-
?
additional information
?
-
apoptosome formation and caspase-9 activation under oxidative stress, oxidative modification of caspase-9 mediates interaction with APAF-1 and promotes its auto-cleavage and activation
-
-
?
additional information
?
-
ligand-independent caspase-9-dependent spontaneous apoptosis triggered by knockdown of the cellular-FLICE inhibitory protein (c-FLIP) using small interfering RNA (siRNA)
-
-
?
additional information
?
-
-
caspase-9 cleaves the the LEHD sequence
-
-
?
additional information
?
-
-
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
-
-
?
additional information
?
-
-
as a cleaved dimer, the L2 loop from one half of the dimer is able to interact with the L2' loop from the other half in the presence of substrate, similarly to other caspases. In this state, the protein is catalytically competent to process substrate. Like other caspases, caspase-9 recognizes its substrates and cleaves after specific aspartic acid residues
-
-
?
additional information
?
-
-
catalytic Cys299 residue with a His249 involved in catalysis
-
-
?
additional information
?
-
-
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
-
-
?
additional information
?
-
-
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
-
-
?
additional information
?
-
-
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
-
-
?
additional information
?
-
-
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
-
-
?
additional information
?
-
-
caspase-9 is dispensable for activation of cyclin-dependent kinase 5 during cell death
-
-
?
additional information
?
-
-
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
-
-
?
additional information
?
-
-
differential caspase-9-dependent signaling pathway between tumor necrosis factor receptor- and Fas-mediated hepatocyte apoptosis
-
-
?
additional information
?
-
-
local apoptosis of lymphatic tissue in polymicrobial sepsis is processed dependent on caspase-9
-
-
?
additional information
?
-
-
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
-
-
?
additional information
?
-
mitochondria-dependent caspase activation for mediation of isorhamnetin-induced apoptosis
-
-
?
additional information
?
-
phosphorylation of caspase-9 at Thr125 by the protein kinase DYRK1A inhibits its cleavage and activation
-
-
?
additional information
?
-
-
phosphorylation of caspase-9 at Thr125 by the protein kinase DYRK1A inhibits its cleavage and activation
-
-
?
additional information
?
-
-
caspase-9 plays a marginal role in serum starvation-induced apoptosis. Caspase-9 sequestration represents a cellular mechanism to impair apoptosome assembly
-
-
?
additional information
?
-
-
caspase-9 plays a marginal role in serum starcvation-induced apoptosis. caspase-9 sequestration represents a cellular mechanism to impair apoptosome assembly
-
-
?
additional information
?
-
-
effect of fluoride treatment (NaF) on osteoblast proliferation, apoptosis and expression of caspase-9 mRNA in vitro
-
-
?
additional information
?
-
-
NO generated during hypoxia leads to activation of caspase-9 and results in initiation of caspase-cascade-dependent hypoxic neuronal death
-
-
?
additional information
?
-
-
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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(3S,6S,10aS)-6-(L-alanylamino)-N-(diphenylmethyl)-5-oxodecahydropyrrolo[1,2-a]azocine-3-carboxamide
-
-
(3S,6S,8aS)-6-(L-alanylamino)-N-(diphenylmethyl)-5-oxooctahydroindolizine-3-carboxamide
-
-
(3S,6S,9aS)-6-(L-alanylamino)-N-(diphenylmethyl)-5-oxooctahydro-1H-pyrrolo[1,2-a]azepine-3-carboxamide
-
-
acetyl-DVAD fluoromethyl ketone
-
prediction of the tertiary structure of a caspase-9/inhibitor complex
ATP
-
enzyme activity is inhibited in both normoxic and hypoxic groups. The IC50 increases 5fold following hypoxia, suggesting a hypoxia-induced modification of the ATP binding site. 70% inhibition by 1 mM
benzyloxycarbonyl-Ile-Glu-Thr-Asp-fluoromethylketone
-
-
benzyloxycarbonyl-LEHD-fluoromethylketone
benzyloxycarbonyl-Leu-Glu-His-Asp-fluoromethylketone
benzyloxycarbonyl-VAD-fluoromethylketone
benzyloxycarbonyl-VAE-fluoromethylketone
-
-
benzyloxycarbonyl-Val-Asp-Val-Ala-Asp-fluoromethylketone
-
-
biotin-Val-Ala-Asp-fluoromethyl ketone
i.e. biotin-VAD-fmk, presence or absence of 50 microM inhibitor, caspase-9 activation analyzed by affinity labelling and immunoblotting
cadmium
anti-apoptotic cell survival function of cadmium, cadmium inhibits apoptosis induced by benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE) at non-cytotoxic concentrations, 40% and 52% inhibition at 10 and 20 microM cadmium chloride, respectively
caspase-9S
-
transfection of renal epithelial cells with the dominant-negative inhibitor caspase-9S
-
cowpox serpin CrmA
-
the Ki-value is below 2.3 nM
-
cytochrome c
-
enzyme activity is inhibited in both normoxic and hypoxic groups. The IC50 increases 1.5fold following hypoxia, suggesting a hypoxia-induced modification of the cytochrome binding site. 70% inhibition by 0.003 mM
L-alanyl-L-valyl-L-prolyl-L-isoleucinamide
-
-
N-(2-amino-2-oxoethyl)-1-[2-(2,4-dichlorophenyl)ethyl]-4-(3,3-diphenylpropyl)-N-[2-(2-fluorophenyl)ethyl]-3,7-dioxo-1,4-diazepane-5-carboxamide
5 microM for cell treatment, cells harvested after 24, 48, and 72 h, 51% inhibition of caspase-3 activity in SAOS-2 cells
N-(2-amino-2-oxoethyl)-1-[2-(2,4-dichlorophenyl)ethyl]-4-(3,3-diphenylpropyl)-N-[2-(2-methoxyphenyl)ethyl]-3,7-dioxo-1,4-diazepane-5-carboxamide
5 microM for cell treatment, cells harvested after 24, 48, and 72 h, 1% inhibition of caspase-3 activity in SAOS-2 cells
N-(2-amino-2-oxoethyl)-1-[2-(2,4-dichlorophenyl)ethyl]-4-(3,3-diphenylpropyl)-N-[2-(4-fluorophenyl)ethyl]-3,7-dioxo-1,4-diazepane-5-carboxamide
5 microM for cell treatment, cells harvested after 24, 48, and 72, 34% inhibition of caspase-3 activity in SAOS-2 cells
N-(2-amino-2-oxoethyl)-N-(2-cyclopropylethyl)-1-[2-(2,4-dichlorophenyl)ethyl]-4-(3,3-diphenylpropyl)-3,7-dioxo-1,4-diazepane-5-carboxamide
5 microM for cell treatment, cells harvested after 24, 48, and 72 h, 16% inhibition of caspase-3 activity in SAOS-2 cells
N-(2-amino-2-oxoethyl)-N-butyl-1-[2-(2,4-dichlorophenyl)ethyl]-4-(3,3-diphenylpropyl)-3,7-dioxo-1,4-diazepane-5-carboxamide
5 microM for cell treatment, cells harvested after 24, 48, and 72 h for caspase activity assay, 45% inhibition of caspase-3 activity in SAOS-2 cells
N-(2-amino-2-oxoethyl)-N-[2-(4-chlorophenyl)ethyl]-1-[2-(2,4-dichlorophenyl)ethyl]-4-(3,3-diphenylpropyl)-3,7-dioxo-1,4-diazepane-5-carboxamide
5 microM for cell treatment, cells harvested after 24, 48, and 72 h, 2% inhibition of caspase-3 activity in SAOS-2 cells
N-benzyloxycarbonyl-Val-Ala-Asp fluoromethyl ketone
i.e. Z-VAD-FMK, treatment with 100 microM caspase inhibitor in combination with 100 microM cordycepin for 24 h suppresses sub-G1 phase in MA-10 cells
N-Fmoc-S-2-(2'-octyl)alanine
-
-
N-Fmoc-S-2-(2'-pentyl)alanine
-
-
N-[2-(acetylamino)ethyl]-N-(2-amino-2-oxoethyl)-1-[2-(2,4-dichlorophenyl)ethyl]-4-(3,3-diphenylpropyl)-3,7-dioxo-1,4-diazepane-5-carboxamide
5 microM for cell treatment, cells harvested after 24, 48, and 72 h, 22% inhibition of caspase-3 activity in SAOS-2 cells
Pen-1-XBIR3
-
caspase-9 is inhibited by unilateral intravitreal injection of highly specific X-linked inhibitor of apoptosis (IAP) baculoviral IAP repeat 3 (XBIR3) domain linked to the cell transduction peptide penetratin 1 (Pen-1) after ballistic injury
-
Q-VD-OPH
i.e. (3S)-5-(2,6-difluorophenoxy)-3-[[(2S)-2-(isoquinoline-3-carbonylamino)-3-methylbutanoyl]amino]-4-oxopentanoic acid, cell treatment with the broad-spectrum caspase inhibitor Q-VD-OPH (concentration 30 microM) prior to induction of differentiation
RQIKIWFQNRRMKWKKGG-N-[2-(2,4-dichlorophenyl)ethyl]glycyl-N-(3,3-diphenylpropyl)glycyl-N2-[2-(2,4-dichlorophenyl)ethyl]glycinamide
i.e. PEN-1, modified compound with peptide bridge, 5 microM for cell treatment, shows low inhibitory activity of caspase-3
XIAP
-
can antagonise caspase-9 activity and stabilises its interaction with the apoptosome. Caspase-3 cleaves XIAP into fragments that retain their inhibitory potential towards caspases-3 or -9, thereby eliminating sterical hindrance that may prevent parallel inhibition of caspases-3 and -9 by XIAP
-
XIAP-BIR3
-
a natural caspase-9 inhibitor that binds at the dimer interface keeping the enzyme in an inactive monomeric state, binding to the enzyme involves the alpha5 helix of XIAP-BIR3
-
Z-IETD-fluoromethylketone
-
a caspase-8 specific inhibitor, delays the activation of caspase-3 and caspase-9 significantly
Z-LEHD-fluoromethylketone
Z-VAD-fluoromethylketone
-
a pan-caspase inhibitor
Zn2+
-
mixed-tpe inhibition, kinetics and mechanism of zinc-mediated inhibition of caspase-9, overview. Two distinct zinc-binding sites on caspase-9, the first site, composed of H237, C239, and C287, includes the active site dyad and is primarily responsible for zinc-mediated inhibition. The second binding site at C272 is distal from the active site. EDTA can hinder enzyme inhibition by Zn2+. Zinc-mediated inhibition does not influence the overall structure of caspase-9 monomers. Each wild-type caspase-9 monomer binds two zinc ions. Caspase-9 variants in which the active-site residues are replaced, C287A or H237A, bind just one zinc
benzyloxycarbonyl-LEHD-fluoromethylketone
cell transfection with siRNA against the cellular-FLICE inhibitory protein (c-FLIP) followed by the addition of the caspase-9 inhibitor benzyloxycarbonyl-Leu-Glu-His-Asp-fluoromethylketone protects the cells from spontaneous apoptosis, indicates that c-FLIP siRNA-triggered apoptosis occurrs by a caspase-9-dependent process, inhibitor concentration of 20 microM for 48 h, apoptosis determined by counting fragmented nuclei using fluorescent dyes, caspase-9 activation shown by Western blot
benzyloxycarbonyl-LEHD-fluoromethylketone
i.e. z-LEHD-FMK, inhibitor effect on apoptosis induced by high linear energy transfer (LET) radiation, induction of apoptosis investigated at 48 h after 10 day irradiation in the presence of 2-100 microM inhibitor concentration, caspase-9 inhibitor suppresses caspase-3 activation and apoptosis induction by radiation to a greater extent than caspase-8 inhibitor
benzyloxycarbonyl-LEHD-fluoromethylketone
-
-
benzyloxycarbonyl-LEHD-fluoromethylketone
i.e. z-LEHD-FMK, specific caspase-9 inhibitor, concentration of 50 microM, inhibitor effect on isorhamnetin-induced apoptosis, cells exposed to DMSO or 40 microM isorhamnetin for 48 h
benzyloxycarbonyl-Leu-Glu-His-Asp-fluoromethylketone
-
-
benzyloxycarbonyl-Leu-Glu-His-Asp-fluoromethylketone
i.e. z-LEHD-FMK, inhibitor concentration 100 microM
benzyloxycarbonyl-Leu-Glu-His-Asp-fluoromethylketone
-
-
benzyloxycarbonyl-VAD-fluoromethylketone
-
t1/2 at 0.001 mM is 3.9 s
benzyloxycarbonyl-VAD-fluoromethylketone
-
-
benzyloxycarbonyl-VAD-fluoromethylketone
i.e. Z-VAD-FMK, in vitro oocyte meiosis and fragmentation analyzed by treatment with concentrations of 50 and 100 microM, transition from metaphase I to metaphase II accelerated in oocytes, comparative treatment with the apoptotic inducer doxorubicin (DXR)
PGA-1
PGA-peptoid conjugate, inhibitor of apoptotic protease activating factor 1 (Apaf-1) coupled to poly-L-glutamic acid (PGA), at concentrations of 50 and 100 microM inhibition of caspase-3 activity, reaches values up to 100% at 50 microM drug after 48 h in HeLa-cells and and after 72 h in SAOS-2 cells
PGA-1
-
PGA-peptoid 1, inhibitor (peptoid 1) of apoptotic protease activating factor 1 (Apaf-1) coupled to poly-L-glutamic acid (PGA)
Z-LEHD-fluoromethylketone
-
a caspase-9 inhibitor
Z-LEHD-fluoromethylketone
-
a caspase-9 specific inhibitor, inhibits caspase-9 activation completely
additional information
-
inhibition of caspase-9 enhances the viability of the CHO cells in both batch and fed-batch suspension cultures
-
additional information
rituximab-induced apoptosis involved in the activation of caspase-9 can be blocked by Bcl-xL overexpression
-
additional information
DYRK1A-dependent phosphorylation of Thr125 blocked by the kinase inhibitor harmine
-
additional information
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DYRK1A-dependent phosphorylation of Thr125 blocked by the kinase inhibitor harmine
-
additional information
caspase-9/-3 activation in differentiated cells, inhibited by protein kinase C (PKC) and the mitogen activated protein kinase (MEK) signaling pathways
-
additional information
-
development, design and synthesis, of three types of stabilized peptides derived from the alpha5 helix of inhibitor XIAP-BIR3, using incorporation of amino-isobutyric acid, the avian pancreatic polypeptide-scaffold or aliphatic staples, overview. The stabilized peptides are helical in solution and achieve good inhibition, indicating that this allosteric site at the caspase-9 dimerization interface is regulatable with low-molecular weight synthetic ligands and is thus a druggable site. Other caspases, which are not regulated by dimerization, are not inactivated by these peptides
-
additional information
-
caspase-3 can bind to the nucleotide binding domain of Apaf-1 on the apoptosome backbone. Binding eliminates the close association of caspase-9 with the nucleotide binding domain of Apaf-1, resulting in its inactivation
-
additional information
-
no inhibition by Co2+, PB2+, and Cd2+
-
additional information
activation of caspase-9 by Cd2+ is inhibited by treatment with the herbal drug Hwanggunchungyitang (HGCYT) in a dose-dependent manner, pretreatement of cells with 0.01-1 mg/ml inhibitor for 1 h, treatment with 10 microM Cd2+ for 24 h
-
additional information
the protein kinase DYRK1A is a negative regulator of the intrinsic apoptotic pathway in the developing retina by phosphorylating caspase-9 on the inhibitory threonine residue 125 to prevent activation
-
additional information
-
the protein kinase DYRK1A is a negative regulator of the intrinsic apoptotic pathway in the developing retina by phosphorylating caspase-9 on the inhibitory threonine residue 125 to prevent activation
-
additional information
-
atorvastatin-mediated apoptosis of hepatic stellate cells (HSCs) can be bocked by co-treatment with mevalonic acid and U0126, an activator of the extracellular signal-regulated protein kinase (ERK1/2)
-
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additional information
analysis of apoptosome inhibitors, improvement by chemical modifications for better increase of cellular penetration and efficient prevention of cell death, evaluation of cellular apoptosis by flow cytometry, immunohistochemistry, caspase activation assay
additional information
caspase-9 identified as a substrate of the protein kinase DYRK1A, in vitro translation and immunoprecipitation of FLAG-DYRK1A in absence or presence of kinase inhibitors analyzed, the kinase inhibitor harmine prevents inhibitory phosphorylation of caspase-9 on threonine residue 125, depletion of DYRK1A by RNA silencing inhibits phosphorylation of caspase-9 on Thr125 in cellular assays, co-expression analysis shows interaction between DYRK1A with caspase-9
additional information
-
caspase-9 identified as a substrate of the protein kinase DYRK1A, in vitro translation and immunoprecipitation of FLAG-DYRK1A in absence or presence of kinase inhibitors analyzed, the kinase inhibitor harmine prevents inhibitory phosphorylation of caspase-9 on threonine residue 125, depletion of DYRK1A by RNA silencing inhibits phosphorylation of caspase-9 on Thr125 in cellular assays, co-expression analysis shows interaction between DYRK1A with caspase-9
additional information
contribution of the death receptor and mitochondrial (intrinsic) pathways to apoptosis in follicular lymphoma cells induced by the chimeric mouse-human anti-CD20 antibody rituximab, time course of caspase activation, overexpression of caspase-9 inhibits the rituximab-induced activation of effector proteases (caspase-3, caspase-6 and caspase-7), rituximab-induced release of cytochrome c and collapse of mitochondrial membrane potential regulated by caspase-9
additional information
cytotoxiciy of Vibrio vulnificus cytolysin (VVC) analyzed by treatment of cell cultures with recombinant VVC protein (rVVC), recombinant Vibrio vulnificus cytolysin (rVVC) induces apoptosis in a time- and dose-dependent manner, apoptosis induced by recombinant Vibrio vulnificus cytolysin (rVVC) mediated by caspase-9 activation rather than caspase-8 activation
additional information
-
cytotoxiciy of Vibrio vulnificus cytolysin (VVC) analyzed by treatment of cell cultures with recombinant VVC protein (rVVC), recombinant Vibrio vulnificus cytolysin (rVVC) induces apoptosis in a time- and dose-dependent manner, apoptosis induced by recombinant Vibrio vulnificus cytolysin (rVVC) mediated by caspase-9 activation rather than caspase-8 activation
additional information
genotyping of caspase-9 by PCR analysis, control and patient sample genotype frequencies distributed according to Hardy-Weinberg equilibrium, clinical characteristics and genotypes, evaluation of a single nucleotide polymorphism (SNP) in the caspase-9 gene of multiple sclerosis patients from Southern Italy, presence of the G/G genotype identified as a higher risk factor in the analyzed multiple sclerosis (MS) population, differential caspase-9 production related to the severity of multiple sclerosis
additional information
-
genotyping of caspase-9 by PCR analysis, control and patient sample genotype frequencies distributed according to Hardy-Weinberg equilibrium, clinical characteristics and genotypes, evaluation of a single nucleotide polymorphism (SNP) in the caspase-9 gene of multiple sclerosis patients from Southern Italy, presence of the G/G genotype identified as a higher risk factor in the analyzed multiple sclerosis (MS) population, differential caspase-9 production related to the severity of multiple sclerosis
additional information
hydrogen peroxide application leads to activation of caspase-9 and apoptosis, promoted interaction between caspase-9 and apoptotic protease-activating factor 1 (APAF-1), thiol-oxidant diamide reveals auto-cleavage of caspase-9 and interaction of caspase-9 and APAF-1, formation of disulfide-linked complexes facilitated, in vitro analysis of a mitochondria-free system, point mutation at C403 of caspase-9 impairs caspase-9 activation induced by H2O2, interaction with APAF-1 diminished by impaired disulfide formation, mutant analysis shows that oxidative modification of caspase-9 contributes to the formation of the apoptosome under oxidative stress
additional information
knockdown of the cellular-FLICE inhibitory protein (c-FLIP) using small interfering RNA (siRNA) triggers ligand-independent caspase-9-dependent spontaneous apoptosis, proliferation of MCF-7 breast cancer cells decreased
additional information
mechanisms of adenosine-induced apoptosis in human colonic cancer cells, cell viability, DNA laddering, expression analysis of adenosine receptors, overexpression of A2a adenosine receptors, determination of mitochondrial membrane potentials, adenosine disrupts mitochondrial membrane potentials and activates caspase-9 and caspase-3, but not caspase-8
additional information
-
mechanisms of adenosine-induced apoptosis in human colonic cancer cells, cell viability, DNA laddering, expression analysis of adenosine receptors, overexpression of A2a adenosine receptors, determination of mitochondrial membrane potentials, adenosine disrupts mitochondrial membrane potentials and activates caspase-9 and caspase-3, but not caspase-8
additional information
mechanisms of apoptosis induced by high linear energy transfer (LET) radiation, irradiation with X-rays, C-ion, or Fe-ion beams, apoptosis quantified with Hoechst 33342 staining, activation of caspase-3 analyzed by Western blot and flow cytometry, poly (ADP-ribose) polymerase (PARP) cleavage, caspase-9 inhibitor suppresses caspase-3 activation and induction of apoptosis, high linear energy transfer (LET) radiation enhances apoptosis by activation of caspase-3 through caspase-9, even in the presence of mp53 protein
additional information
-
mechanisms of apoptosis induced by high linear energy transfer (LET) radiation, irradiation with X-rays, C-ion, or Fe-ion beams, apoptosis quantified with Hoechst 33342 staining, activation of caspase-3 analyzed by Western blot and flow cytometry, poly (ADP-ribose) polymerase (PARP) cleavage, caspase-9 inhibitor suppresses caspase-3 activation and induction of apoptosis, high linear energy transfer (LET) radiation enhances apoptosis by activation of caspase-3 through caspase-9, even in the presence of mp53 protein
additional information
mechanisms of apoptosis induced by ionizing radiation on cell lines with a different status of p53 (TP53 tumor suppressor gene), activity of initial caspases (-8 and -9) analyzed by Western-Blot of whole-cell lysates and mitochondrial fractions, cells lacking the p53 protein show activation of caspase-8 prior to activation of caspase-9, cells harboring the p53 protein show a simultaneous activation of both initial caspases, extrinsic (caspase-8 dependent) and intrinsic (caspase-9 dependent) pathways activated upon exposure ionizing radiation regardless to the status of p53 protein
additional information
-
mechanisms of apoptosis induced by ionizing radiation on cell lines with a different status of p53 (TP53 tumor suppressor gene), activity of initial caspases (-8 and -9) analyzed by Western-Blot of whole-cell lysates and mitochondrial fractions, cells lacking the p53 protein show activation of caspase-8 prior to activation of caspase-9, cells harboring the p53 protein show a simultaneous activation of both initial caspases, extrinsic (caspase-8 dependent) and intrinsic (caspase-9 dependent) pathways activated upon exposure ionizing radiation regardless to the status of p53 protein
additional information
mechanisms of apoptosis induced in response to marine sponge extracts of Polymastia janeirensis, flow cytometry analysis, assessment of glioma cell viability, dose-dependent increase in ROS production, inhibitor studies to determine whether the extracts activate the extrinsic or intrinsic pathways of apoptosis, marine sponge extracts of Polymastia janeirensis induce oxidative cell death mediated through the caspase-9 pathway
additional information
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mechanisms of apoptosis induced in response to marine sponge extracts of Polymastia janeirensis, flow cytometry analysis, assessment of glioma cell viability, dose-dependent increase in ROS production, inhibitor studies to determine whether the extracts activate the extrinsic or intrinsic pathways of apoptosis, marine sponge extracts of Polymastia janeirensis induce oxidative cell death mediated through the caspase-9 pathway
additional information
protective effects of cadmium on apoptosis induced by benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE), inhibition of BPDE-induced apoptosis by cadmium is associated with downregulation of caspase-9 activation, cadmium-induced inhibition of apoptosis associated with downregulation of caspase-9 activation, 40% and 52% inhibition of apoptosis after pre-treatment of cells with 10 and 20 microM cadmium chloride, respectively
additional information
-
protective effects of cadmium on apoptosis induced by benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE), inhibition of BPDE-induced apoptosis by cadmium is associated with downregulation of caspase-9 activation, cadmium-induced inhibition of apoptosis associated with downregulation of caspase-9 activation, 40% and 52% inhibition of apoptosis after pre-treatment of cells with 10 and 20 microM cadmium chloride, respectively
additional information
proteomic analysis of caspase-9-associated protein complexes, one-dimensional gel electrophoresis and tandem mass spectrometry, 24 differential caspase-9 interactors identified, assigned to cytoskeletal organization, cell motility, catalytic activity, transcription and apoptosis, galectin-3, swiprosin-1 and the membrane-cytoskeleton linkers ezrin/radixin/moesin identified as novel caspase-9 interactors, co-immunoprecipitation and Western blot to confirm interaction of caspase-9 with identified binding partners
additional information
RC-RNase-induced caspase-9/-3-mediated cytotoxicity in undifferentiated and differentiated cells, cell differentiation and adhesion assays, cell proliferation assays, caspase-9/-3-mediated cytotoxicity can be induced in differentiated cells that are pretreated with inhibitors of protein kinase C (PKC) or mitogen activated protein kinase (MEK), caspases-9/-3-mediated cytotoxicity in differentiated cells inhibited by protein kinase C (PKC) and the mitogen activated protein kinase (MEK) signaling pathways
additional information
analysis of oocytes from prophase I onwards, inhibition of caspase activity accelerates transition from metaphase I to metaphase II, caspase-9 and caspase-3 detected along the meiotic spindle, similar amounts of cleaved caspases in healthy and fragmented oocytes, caspase inhibition does not prevent doxorubicin-induced apoptosis, cleaved caspases probably dispensable for final oocyte death, potential involvement in the regulation of oocyte maturation
additional information
-
analysis of oocytes from prophase I onwards, inhibition of caspase activity accelerates transition from metaphase I to metaphase II, caspase-9 and caspase-3 detected along the meiotic spindle, similar amounts of cleaved caspases in healthy and fragmented oocytes, caspase inhibition does not prevent doxorubicin-induced apoptosis, cleaved caspases probably dispensable for final oocyte death, potential involvement in the regulation of oocyte maturation
additional information
apoptotic mechanism of the flavanoid isorhamnetin, isorhamnetin induces mitochondria-dependent caspase activation cascade, caspase inhibitors block isorhamnetin-induced apoptosis, increased cleavage of caspase-9 shown by Western blot analyses of isorhamnetin-treated cells, cytotoxicity assay, TUNEL assay, DNA fragmentation assay, measurement of mitochondrial membrane potential
additional information
caspase-9 is responsible for the activation of caspase-3 in differentiating myoblasts, decreased caspase-9 levels due to RNA interference prevents caspase-3 activation and impairs muscle differentiation, release of cytochrome c not observed, novel mechanism of caspase-9 activation during muscle differentiation, apoptotic nuclear morphology assessed by DAPI staining, quantification of muscle-cell differentiation, mitochondrial-membrane depolarisation, cell fractionation, immunoblotting
additional information
determination of caspase-9 auto-processing in a cell-free system, phosphorylation of caspase-9 analyzed by Western blot, phosphorylation of caspase-9 by casein kinase 2 (CK2) on a serine near the site of caspase-8 cleavage, CK2 modification of Ser348 on caspase-9 lowers the susceptibility of caspase-9 to cleavage but does not affect caspase-9 auto-processing, substitution of Ser348 abolishes phosphorylation but not cleavage, phosphatase inhibitors delay apoptosis induced by tumor necrosis factor (TNF)-alpha, inhibition of kinase activity or loss of the kinase accelerates apoptosis and promotes early caspase-9 activation in response to TNF-alpha, modification of pro-caspase-9 in the vicinity of its processing motif protects the protease from inappropriate activation by other caspases
additional information
-
determination of caspase-9 auto-processing in a cell-free system, phosphorylation of caspase-9 analyzed by Western blot, phosphorylation of caspase-9 by casein kinase 2 (CK2) on a serine near the site of caspase-8 cleavage, CK2 modification of Ser348 on caspase-9 lowers the susceptibility of caspase-9 to cleavage but does not affect caspase-9 auto-processing, substitution of Ser348 abolishes phosphorylation but not cleavage, phosphatase inhibitors delay apoptosis induced by tumor necrosis factor (TNF)-alpha, inhibition of kinase activity or loss of the kinase accelerates apoptosis and promotes early caspase-9 activation in response to TNF-alpha, modification of pro-caspase-9 in the vicinity of its processing motif protects the protease from inappropriate activation by other caspases
additional information
protective effect of the herbal drug Hwanggunchungyitang (HGCYT) against activation of caspase-9 by Cd2+, activity of caspase-9 measured by colorimetric assay and Western Blot analysis
additional information
protein kinase DYRK1A is a negative regulator of the intrinsic apoptotic pathway in the developing retina, DYRK1A phosphorylates caspase-9 on threonine residue 125, phosphorylation crucial to protect retina cells from apoptotic cell death, dysregulation of the apoptotic response in differentiating neurons with an imbalance effects of DYRK1A gene-dosage participates in the neuropathology of diseases
additional information
-
protein kinase DYRK1A is a negative regulator of the intrinsic apoptotic pathway in the developing retina, DYRK1A phosphorylates caspase-9 on threonine residue 125, phosphorylation crucial to protect retina cells from apoptotic cell death, dysregulation of the apoptotic response in differentiating neurons with an imbalance effects of DYRK1A gene-dosage participates in the neuropathology of diseases
additional information
value of an inducible caspase-9-based safety switch to halt an ongoing immune attack, retroviral transduction of T cells, induction and analysis of apoptosis, depletion of transduced T cells determined by flow cytometric analysis of GFP expression, in vivo assessment of the inducible caspase-9 suicide switch, immunohistochemistry, evaluation of this conditional safety switch in clinical trials of adoptive cell therapy
additional information
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value of an inducible caspase-9-based safety switch to halt an ongoing immune attack, retroviral transduction of T cells, induction and analysis of apoptosis, depletion of transduced T cells determined by flow cytometric analysis of GFP expression, in vivo assessment of the inducible caspase-9 suicide switch, immunohistochemistry, evaluation of this conditional safety switch in clinical trials of adoptive cell therapy
additional information
Western blot analysis reveals cordycepin-induced expression of caspase-9, activation of caspase-3 and caspase-7, but not of caspase-8 in a time- and dose-dependent manner, cordycepin-induced apoptosis acts through a caspase-9 and caspase-3 and caspase-7 dependent pathway
additional information
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Western blot analysis reveals cordycepin-induced expression of caspase-9, activation of caspase-3 and caspase-7, but not of caspase-8 in a time- and dose-dependent manner, cordycepin-induced apoptosis acts through a caspase-9 and caspase-3 and caspase-7 dependent pathway
additional information
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atorvastatin induces apoptosis in hepatic stellate cells (HSCs), atorvastatin-mediated apoptosis is blocked by co-application of mevalonic acid and U0126, an activator of the extracellular signal-regulated protein kinase (ERK1/2), increased activity of caspase-9 to 407% and of caspase-3 to 540% in cells treated with atorvastatin, flow cytometry, laser-scanning microscopy, Western blot, electrophoresis mobility shift assay, pathway of apoptosis induced by atorvastatin in hepatic stellate cells (HSCs) summarized
additional information
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increase in osteoblast apoptosis observed after 24 and 72 h treatment in response to the lowest dose of sodium fluoride (0.5 mg/l), osteoblast apoptosis also increased in response to higher doses, mRNA of caspase-9 increased in response to sodium fluoride treatment (5 mg/l) for 72 h, morphological and histochemical characterization of osteoblasts, cell proliferation and apoptosis assays, quantification of mRNA expression of caspase-3 and caspase-9 by real time PCR
additional information
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the poly-L-glutamic acid (PGA) derivative PGA-1 is capable of reducing hypoxia-induced apoptosis in primary culture cardiomyocytes
additional information
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increased activity of caspase-9 during hypoxia, significant increase in the phophorylation on Ser196 during hypoxia, modification at Ser196 results in alterations of proteolytic cleavage of procaspase-9 and caspase-9 activity
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Duan H.; Orth K.; Chinnaiyan A.M.; Poirier G.G.; Froelich C.J.; He W.W.; Dixit V.M.
ICE-LAP6, a novel member of the ICE/Ced-3 gene family, is activated by the cytotoxic T cell protease granzyme B
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The Ced-3/interleukin 1beta converting enzyme-like homolog Mch6 and the lamin-cleaving enzyme Mch2alpha are substrates for the apoptotic mediator CPP32
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A caspase-9 variant missing the catalytic site is an endogenous inhibitor of apoptosis
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Inhibition of caspase-9 through phosphorylation at Thr 125 by ERK MAPK
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Regulation of cell death protease caspase-9 by phosphorylation
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Martelli, A.M.; Cappellini, A.; Tazzari, P.L.; Billi, A.M.; Tassi, C.; Ricci, F.; Fala, F.; Conte, R.
Caspase-9 is the upstream caspase activated by 8-methoxypsoralen and ultraviolet-A radiation treatment of Jurkat T leukemia cells and normal T lymphocytes
Haematologica
89
471-479
2004
Homo sapiens
brenda
Kasili, P.M.; Song, J.M.; Vo-Dinh, T.
Optical sensor for the detection of caspase-9 activity in a single cell
J. Am. Chem. Soc.
126
2799-2806
2004
Homo sapiens
brenda
Akasaki, Y.; Liu, G.; Matunda, H.H.; Ng, H.; Yuan, X.; Zeng, Z.; Black, K.L.; Yu, J.S.
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
J. Biol. Chem.
281
6165-6174
2006
Homo sapiens
brenda
Peluffo, M.C.; Young, K.A.; Stouffer, R.L.
Dynamic expression of caspase-2, -3, -8, and -9 proteins and enzyme activity, but not messenger ribonucleic acid, in the monkey corpus luteum during the menstrual cycle
J. Clin. Endocrinol. Metab.
90
2327-2335
2006
Macaca mulatta
brenda
Oberholzer, C.; Tschoeke, S.K.; Moldawer, L.L.; Oberholzer, A.
Local thymic caspase-9 inhibition improves survival during polymicrobial sepsis in mice
J. Mol. Med.
84
389-395
2006
Mus musculus
brenda
Wang, P.; Shi, T.; Ma, D.
Cloning of a novel human caspase-9 splice variant containing only the CARD domain
Life Sci.
79
934-940
2006
Homo sapiens (P55211), Homo sapiens
brenda
Imao, M.; Nagaki, M.; Imose, M.; Moriwaki, H.
Differential caspase-9-dependent signaling pathway between tumor necrosis factor receptor- and Fas-mediated hepatocyte apoptosis in mice
Liver Int.
26
137-146
2006
Mus musculus
brenda
Maglione, V.; Cannella, M.; Gradini, R.; Cislaghi, G.; Squitieri, F.
Huntingtin fragmentation and increased caspase 3, 8, and 9 activities in lymphoblasts with heterozygous and homozygous Huntington's disease mutation
Mech. Ageing Dev.
127
213-216
2006
Homo sapiens
brenda
Yin, Q.; Park, H.H.; Chung, J.Y.; Lin, S.C.; Lo, Y.C.; da Graca, L.S.; Jiang, X.; Wu, H.
Caspase-9 holoenzyme is a specific and optimal procaspase-3 processing machine
Mol. Cell
22
259-268
2006
Homo sapiens (P55211)
brenda
Pop, C.; Timmer, J.; Sperandio, S.; Salvesen, G.S.
The apoptosome activates caspase-9 by dimerization
Mol. Cell
22
269-275
2006
Homo sapiens
brenda
Yi, X.; Wang, J.; Seol, D.W.; Dong, Z.
Characterization of cell clones stably transfected with short form caspase-9: apoptotic resistance and Bcl-XL expression
Mol. Cell. Biochem.
282
1-12
2006
Rattus norvegicus
brenda
Mishra, O.P.; Delivoria-Papadopoulos, M.
ATP and cytochrome c-dependent inhibition of caspase-9 activity in the cerebral cortex of newborn piglets
Neurosci. Lett.
364
119-123
2004
Sus scrofa
brenda
Mishra, O.P.; Delivoria-Papadopoulos, M.
Effect of neuronal nitric oxide synthase inhibition on caspase-9 activity during hypoxia in the cerebral cortex of newborn piglets
Neurosci. Lett.
401
81-85
2006
Sus scrofa
brenda
Lemaire, C.; Godefroy, N.; Costina-Parvu, I.; Rincheval, V.; Renaud, F.; Trotot, P.; Bouleau, S.; Mignotte, B.; Vayssiere, J.L.
Caspase-9 can antagonize p53-induced apoptosis by generating a p76(Rb) truncated form of Rb
Oncogene
24
3297-3308
2005
Rattus norvegicus
brenda
Cepero, E.; King, A.M.; Coffey, L.M.; Perez, R.G.; Boise, L.H.
Caspase-9 and effector caspases have sequential and distinct effects on mitochondria
Oncogene
24
6354-6366
2005
Mus musculus
brenda
Sadhukhan, R.; Leone, J.W.; Lull, J.; Wang, Z.; Kletzien, R.F.; Heinrikson, R.L.; Tomasselli, A.G.
An efficient method to express and refold a truncated human procaspase-9: a caspase with activity toward Glu-X bonds
Protein Expr. Purif.
46
299-308
2006
Homo sapiens
brenda
Peluffo, M.C.; Bussmann, L.; Stouffer, R.L.; Tesone, M.
Expression of caspase-2, -3, -8 and -9 proteins and enzyme activity in the corpus luteum of the rat at different stages during the natural estrous cycle
Reproduction
132
465-475
2006
Rattus norvegicus
brenda
Papandile, A.; Tyas, D.; OMalley, D.M.; Warner, C.M.
Analysis of caspase-3, caspase-8 and caspase-9 enzymatic activities in mouse oocytes and zygotes
Zygote
12
57-64
2004
Mus musculus
brenda
Lysiak, J.J.; Zheng, S.; Woodson, R.; Turner, T.T.
Caspase-9-dependent pathway to murine germ cell apoptosis: mediation by oxidative stress, BAX, and caspase 2
Cell Tissue Res.
328
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2007
Mus musculus
brenda
Saikumar, P.; Mikhailova, M.; Pandeswara, S.L.
Regulation of caspase-9 activity by differential binding to the apoptosome complex
Front. Biosci.
12
3343-3354
2007
Rattus norvegicus
brenda
Uchiyama, R.; Kawamura, I.; Fujimura, T.; Kawanishi, M.; Tsuchiya, K.; Tominaga, T.; Kaku, T.; Fukasawa, Y.; Sakai, S.; Nomura, T.; Mitsuyama, M.
Involvement of caspase-9 in the inhibition of necrosis of RAW 264 cells infected with Mycobacterium tuberculosis
Infect. Immun.
75
2894-2902
2007
Mus musculus
brenda
Samraj, A.K.; Keil, E.; Ueffing, N.; Schulze-Osthoff, K.; Schmitz, I.
Loss of caspase-9 provides genetic evidence for the type I/II concept of CD95-mediated apoptosis
J. Biol. Chem.
281
29652-29659
2006
Homo sapiens
brenda
Furuta, K.; Nakayama, K.; Sugimoto, Y.; Ichikawa, A.; Tanaka, S.
Activation of histidine decarboxylase through post-translational cleavage by caspase-9 in a mouse mastocytoma P-815
J. Biol. Chem.
282
13438-13446
2007
Mus musculus
brenda
Chen, M.; Guerrero, A.D.; Huang, L.; Shabier, Z.; Pan, M.; Tan, T.H.; Wang, J.
Caspase-9-induced mitochondrial disruption through cleavage of anti-apoptotic BCL-2 family members
J. Biol. Chem.
282
33888-33895
2007
Homo sapiens
brenda
Martin, M.C.; Allan, L.A.; Mancini, E.J.; Clarke, P.R.
The docking interaction of caspase-9 with ERK2 provides a mechanism for the selective inhibitory phosphorylation of caspase-9 at threonine 125
J. Biol. Chem.
283
3854-3865
2008
Homo sapiens
brenda
Yun, C.Y.; Liu, S.; Lim, S.F.; Wang, T.; Chung, B.Y.; Jiat Teo, J.; Chuan, K.H.; Soon, A.S.; Goh, K.S.; Song, Z.
Specific inhibition of caspase-8 and -9 in CHO cells enhances cell viability in batch and fed-batch cultures
Metab. Eng.
9
406-418
2007
Cricetulus griseus
brenda
Samraj, A.K.; Sohn, D.; Schulze-Osthoff, K.; Schmitz, I.
Loss of caspase-9 reveals its essential role for caspase-2 activation and mitochondrial membrane depolarization
Mol. Biol. Cell
18
84-93
2007
Homo sapiens
brenda
Allan, L.A.; Clarke, P.R.
Phosphorylation of caspase-9 by CDK1/cyclin B1 protects mitotic cells against apoptosis
Mol. Cell
26
301-310
2007
Homo sapiens
brenda
Gyrd-Hansen, M.; Farkas, T.; Fehrenbacher, N.; Bastholm, L.; Hoyer-Hansen, M.; Elling, F.; Wallach, D.; Flavell, R.; Kroemer, G.; Nylandsted, J.; Jaeaettelae, M.
Apoptosome-independent activation of the lysosomal cell death pathway by caspase-9
Mol. Cell. Biol.
26
7880-7891
2006
Mus musculus
brenda
Coen, L.; Le Blay, K.; Rowe, I.; Demeneix, B.A.
Caspase-9 regulates apoptosis/proliferation balance during metamorphic brain remodeling in Xenopus
Proc. Natl. Acad. Sci. USA
104
8502-8507
2007
Xenopus laevis
brenda
Loureiro, B.; Brad, A.M.; Hansen, P.J.
Heat shock and tumor necrosis factor-alpha induce apoptosis in bovine preimplantation embryos through a caspase-9-dependent mechanism
Reproduction
133
1129-1137
2007
Bos taurus
brenda
Kuckleburg, C.J.; Tiwari, R.; Czuprynski, C.J.
Endothelial cell apoptosis induced by bacteria-activated platelets requires caspase-8 and -9 and generation of reactive oxygen species
Thromb. Haemost.
99
363-372
2008
Bos taurus
brenda
Eeva, J.; Nuutinen, U.; Ropponen, A.; Maettoe, M.; Eray, M.; Pellinen, R.; Wahlfors, J.; Pelkonen, J.
The involvement of mitochondria and the caspase-9 activation pathway in rituximab-induced apoptosis in FL cells
Apoptosis
14
687-698
2009
Homo sapiens (P55211)
brenda
Yan, X.; Feng, C.; Chen, Q.; Li, W.; Wang, H.; Lv, L.; Smith, G.W.; Wang, J.
Effects of sodium fluoride treatment in vitro on cell proliferation, apoptosis and caspase-3 and caspase-9 mRNA expression by neonatal rat osteoblasts
Arch. Toxicol.
83
451-458
2008
Rattus norvegicus
brenda
Yi, J.Y.; Hirabayashi, Y.; Choi, Y.K.; Kodama, Y.; Kanno, J.; Han, J.H.; Inoue, T.; Yoon, B.I.
Benzene activates caspase-4 and -12 at the transcription level, without an association with apoptosis, in mouse bone marrow cells lacking the p53 gene
Arch. Toxicol.
83
795-803
2009
Mus musculus
brenda
Day, T.W.; Huang, S.; Safa, A.R.
c-FLIP knockdown induces ligand-independent DR5-, FADD-, caspase-8-, and caspase-9-dependent apoptosis in breast cancer cells
Biochem. Pharmacol.
76
1694-1704
2008
Homo sapiens (P55211)
brenda
Kim, S.J.; Shin, B.G.; Choi, I.Y.; Kim, D.H.; Kim, M.C.; Myung, N.Y.; Moon, P.D.; Lee, J.H.; An, H.J.; Kim, N.H.; Lee, J.Y.; So, H.S.; Park, R.K.; Jeong, H.J.; Um, J.Y.; Kim, H.M.; Hong, S.H.
Hwanggunchungyitang prevents cadmium-induced ototoxicity through suppression of the activation of caspase-9 and extracellular signal-related kinase in auditory HEI-OC1 cells
Biol. Pharm. Bull.
32
213-219
2009
Mus musculus (Q9R0T0)
brenda
Lee, H.J.; Lee, H.J.; Lee, E.O.; Ko, S.G.; Bae, H.S.; Kim, C.H.; Ahn, K.S.; Lu, J.; Kim, S.H.
Mitochondria-cytochrome C-caspase-9 cascade mediates isorhamnetin-induced apoptosis
Cancer Lett.
270
342-353
2008
Mus musculus (Q9R0T0)
brenda
Yamakawa, N.; Takahashi, A.; Mori, E.; Imai, Y.; Furusawa, Y.; Ohnishi, K.; Kirita, T.; Ohnishi, T.
High LET radiation enhances apoptosis in mutated p53 cancer cells through Caspase-9 activation
Cancer Sci.
99
1455-1460
2008
Homo sapiens (P55211), Homo sapiens
brenda
Zuo, Y.; Xiang, B.; Yang, J.; Sun, X.; Wang, Y.; Cang, H.; Yi, J.
Oxidative modification of caspase-9 facilitates its activation via disulfide-mediated interaction with APAF-1
Cell Res.
19
449-457
2009
Homo sapiens (P55211)
brenda
Laguna, A.; Aranda, S.; Barallobre, M.J.; Barhoum, R.; Fernandez, E.; Fotaki, V.; Delabar, J.M.; de la Luna, S.; de la Villa, P.; Arbones, M.L.
The protein kinase DYRK1A regulates caspase-9-mediated apoptosis during retina development
Dev. Cell
15
841-853
2008
Mus musculus (Q9R0T0), Mus musculus
brenda
Arnault, E.; Tosca, L.; Courtot, A.M.; Doussau, M.; Pesty, A.; Finaz, C.; Allemand, I.; Lefevre, B.
Caspase-2(L), caspase-9, and caspase-3 during in vitro maturation and fragmentation of the mouse oocyte
Dev. Dyn.
237
3892-3903
2008
Mus musculus (Q9R0T0), Mus musculus
brenda
Jen, C.Y.; Lin, C.Y.; Leu, S.F.; Huang, B.M.
Cordycepin induced MA-10 mouse Leydig tumor cell apoptosis through caspase-9 pathway
Evid. Based. Complement Alternat. Med.
2009
1-10
2009
Mus musculus (Q9R0T0), Mus musculus
brenda
Seifert, A.; Allan, L.A.; Clarke, P.R.
DYRK1A phosphorylates caspase 9 at an inhibitory site and is potently inhibited in human cells by harmine
FEBS J.
275
6268-6280
2008
Homo sapiens (P55211), Homo sapiens
brenda
Yiang, G.T.; Yu, Y.L.; Hu, S.C.; Chen, M.H.; Wang, J.J.; Wei, C.W.
PKC and MEK pathways inhibit caspase-9/-3-mediated cytotoxicity in differentiated cells
FEBS Lett.
582
881-885
2008
Homo sapiens (P55211)
brenda
Tichy, A.; Zaskodova, D.; Pejchal, J.; Rezacova, M.; Osterreicher, J.; Vavrova, J.; Cerman, J.
Gamma irradiation of human leukaemic cells HL-60 and MOLT-4 induces decrease in Mcl-1 and Bid, release of cytochrome c, and activation of caspase-8 and caspase-9
Int. J. Radiat. Biol.
84
523-530
2008
Homo sapiens (P55211), Homo sapiens
brenda
Conte da Frota, M.L.; Braganhol, E.; Delgado Canedo, A.; Klamt, F.; Apel, M.A.; Mothes, B.; Lerner, C.; Oliveira Battastini, A.M.; Henriques, A.T.; Fonseca Moreira, J.C.
Extracts of marine sponge Polymastia janeirensis induce oxidative cell death through a caspase-9 apoptotic pathway in human U138MG glioma cell line
Invest. New Drugs
27
440-446
2008
Homo sapiens (P55211), Homo sapiens
brenda
McDonnell, M.A.; Abedin, M.J.; Melendez, M.; Platikanova, T.N.; Ecklund, J.R.; Ahmed, K.; Kelekar, A.
Phosphorylation of murine caspase-9 by the protein kinase casein kinase 2 regulates its cleavage by caspase-8
J. Biol. Chem.
283
20149-20158
2008
Mus musculus (Q9R0T0), Mus musculus
brenda
Murray, T.V.; McMahon, J.M.; Howley, B.A.; Stanley, A.; Ritter, T.; Mohr, A.; Zwacka, R.; Fearnhead, H.O.
A non-apoptotic role for caspase-9 in muscle differentiation
J. Cell Sci.
121
3786-3793
2008
Mus musculus (Q9R0T0)
brenda
Yasuda, Y.; Saito, M.; Yamamura, T.; Yaguchi, T.; Nishizaki, T.
Extracellular adenosine induces apoptosis in Caco-2 human colonic cancer cells by activating caspase-9/-3 via A(2a) adenosine receptors
J. Gastroenterol.
44
56-65
2009
Homo sapiens (P55211), Homo sapiens
brenda
de Witte, M.A.; Jorritsma, A.; Swart, E.; Straathof, K.C.; de Punder, K.; Haanen, J.B.; Rooney, C.M.; Schumacher, T.N.
An inducible caspase 9 safety switch can halt cell therapy-induced autoimmune disease
J. Immunol.
180
6365-6373
2008
Mus musculus (Q9R0T0), Mus musculus
brenda
Mondragon, L.; Orzaez, M.; Sanclimens, G.; Moure, A.; Arminan, A.; Sepulveda, P.; Messeguer, A.; Vicent, M.J.; Perez-Paya, E.
Modulation of cellular apoptosis with apoptotic protease-activating factor 1 (Apaf-1) inhibitors
J. Med. Chem.
51
521-529
2008
Rattus norvegicus, Homo sapiens (P55211)
brenda
Andreoli, V.; Trecroci, F.; La Russa, A.; Valentino, P.; Condino, F.; Latorre, V.; Nistico, R.; Pirritano, D.; Del Giudice, F.; Canino, M.; Cittadella, R.; Quattrone, A.
CASP-9: A susceptibility locus for multiple sclerosis in Italy
J. Neuroimmunol.
210
100-103
2009
Homo sapiens (P55211), Homo sapiens
brenda
Checinska, A.; Giaccone, G.; Rodriguez, J.A.; Kruyt, F.A.; Jimenez, C.R.
Comparative proteomics analysis of caspase-9-protein complexes in untreated and cytochrome c/dATP stimulated lysates of NSCLC cells
J. Proteomics
72
575-585
2009
Homo sapiens (P55211)
brenda
Aprigliano, I.; Dudas, J.; Ramadori, G.; Saile, B.
Atorvastatin induces apoptosis by a caspase-9-dependent pathway: an in vitro study on activated rat hepatic stellate cells
Liver Int.
28
546-557
2008
Rattus norvegicus, Rattus norvegicus Wistar
brenda
Zhao, J.F.; Sun, A.H.; Ruan, P.; Zhao, X.H.; Lu, M.Q.; Yan, J.
Vibrio vulnificus cytolysin induces apoptosis in HUVEC, SGC-7901 and SMMC-7721 cells via caspase-9/3-dependent pathway
Microb. Pathog.
46
194-200
2009
Homo sapiens (P55211), Homo sapiens
brenda
Mukherjee, J.J.; Gupta, S.K.; Kumar, S.
Inhibition of benzopyrene-diol-epoxide (BPDE)-induced bax and caspase-9 by cadmium: role of mitogen activated protein kinase
Mutat. Res.
661
41-46
2009
Homo sapiens (P55211), Homo sapiens
brenda
Levenbrown, Y.; Ashraf, Q.M.; Maounis, N.; Mishra, O.P.; Delivoria-Papadopoulos, M.
Phosphorylation of caspase-9 in the cytosolic fraction of the cerebral cortex of newborn piglets following hypoxia
Neurosci. Lett.
447
96-99
2008
Sus scrofa
brenda
Darwish, R.S.; Amiridze, N.S.
Detectable levels of cytochrome C and activated caspase-9 in cerebrospinal fluid after human traumatic brain injury
Neurocrit. Care
12
337-341
2010
Homo sapiens
brenda
Jeong, H.S.; Choi, H.Y.; Lee, E.R.; Kim, J.H.; Jeon, K.; Lee, H.J.; Cho, S.G.
Involvement of caspase-9 in autophagy-mediated cell survival pathway
Biochim. Biophys. Acta
1813
80-90
2011
Homo sapiens
brenda
Abou-Kandil, A.; Chamias, R.; Huleihel, M.; Godbey, W.T.; Aboud, M.
Role of caspase 9 in activation of HTLV-1 LTR expression by DNA damaging agents
Cell Cycle
10
3337-3345
2011
Homo sapiens
brenda
Wu, Y.; Wang, D.; Wang, X.; Wang, Y.; Ren, F.; Chang, D.; Chang, Z.; Jia, B.
Caspase 3 is activated through caspase 8 instead of caspase 9 during H2O2-induced apoptosis in HeLa cells
Cell. Physiol. Biochem.
27
539-546
2011
Homo sapiens
brenda
Mu, Y.; Xiao, X.; Zhang, J.; Ao, J.; Chen, X.
Molecular cloning and functional characterization of caspase 9 in large yellow croaker (Pseudosciaena crocea)
Dev. Comp. Immunol.
34
300-307
2010
Larimichthys crocea
brenda
Li, T.; Cui, Z.B.; Ke, X.X.; Tan, J.; Li, F.F.; Li, T.; Wang, X.W.; Cui, H.J.
Essential role for p53 and caspase-9 in DNA damaging drug-induced apoptosis in neuroblastoma IMR32 cells
DNA Cell Biol.
30
1045-1050
2011
Homo sapiens
brenda
Du, R.H.; Cui, J.T.; Wang, T.; Zhang, A.H.; Tan, R.X.
Trichothecin induces apoptosis of HepG2 cells via caspase-9 mediated activation of the mitochondrial death pathway
Toxicon
59
143-150
2012
Homo sapiens
brenda
Gao, D.; Xu, Z.; Zhang, X.; Wang, H.; Wang, Y.; Min, W.
Molecular cloning, immunohistochemical localization, characterization and expression analysis of caspase-9 from the purse red common carp (Cyprinus carpio) exposed to cadmium
Aquat. Toxicol.
142-143
53-62
2013
Cyprinus carpio
brenda
Bourguet, C.B.; Boulay, P.L.; Claing, A.; Lubell, W.D.
Design and synthesis of novel azapeptide activators of apoptosis mediated by caspase-9 in cancer cells
Bioorg. Med. Chem. Lett.
24
3361-3365
2014
Homo sapiens
brenda
Huber, K.L.; Ghosh, S.; Hardy, J.A.
Inhibition of caspase-9 by stabilized peptides targeting the dimerization interface
Biopolymers
98
451-465
2012
Homo sapiens
brenda
Lu, E.P.; McLellan, M.; Ding, L.; Fulton, R.; Mardis, E.R.; Wilson, R.K.; Miller, C.A.; Westervelt, P.; DiPersio, J.F.; Link, D.C.; Walter, M.J.; Ley, T.J.; Graubert, T.A.
Caspase-9 is required for normal hematopoietic development and protection from alkylator-induced DNA damage in mice
Blood
124
3887-3895
2014
Mus musculus, Mus musculus C57/BL6J
brenda
Brentnall, M.; Rodriguez-Menocal, L.; De Guevara, R.L.; Cepero, E.; Boise, L.H.
Caspase-9, caspase-3 and caspase-7 have distinct roles during intrinsic apoptosis
BMC Cell Biol.
14
32
2013
Mus musculus
brenda
Nie, C.; Luo, Y.; Zhao, X.; Luo, N.; Tong, A.; Liu, X.; Yuan, Z.; Wang, C.; Wei, Y.
Caspase-9 mediates Puma activation in UCN-01-induced apoptosis
Cell Death Dis.
5
e1495
2014
Homo sapiens
brenda
Wuerstle, M.L.; Laussmann, M.A.; Rehm, M.
The central role of initiator caspase-9 in apoptosis signal transduction and the regulation of its activation and activity on the apoptosome
Exp. Cell Res.
318
1213-1220
2012
Homo sapiens
brenda
Blanch, R.J.; Ahmed, Z.; Thompson, A.R.; Akpan, N.; Snead, D.R.; Berry, M.; Troy, C.M.; Scott, R.A.; Logan, A.
Caspase-9 mediates photoreceptor death after blunt ocular trauma
Invest. Ophthalmol. Vis. Sci.
55
6350-6357
2014
Rattus norvegicus
brenda
Huber, K.L.; Hardy, J.A.
Mechanism of zinc-mediated inhibition of caspase-9
Protein Sci.
21
1056-1065
2012
Homo sapiens
brenda
Wei, X.; Li, Q.; Han, Z.; Lin, D.; Yu, P.
Differences in caspase-8 and -9 activity and sperm motility in infertile males of Li nationality in China
Int. J. Clin. Exp. Med.
8
4721-4726
2015
Homo sapiens (P55211), Homo sapiens
brenda
Diaconu, I.; Ballard, B.; Zhang, M.; Chen, Y.; West, J.; Dotti, G.; Savoldo, B.
Inducible caspase-9 selectively modulates the toxicities of CD19-specific chimeric antigen receptor-modified T cells
Mol. Ther.
25
580-592
2017
Homo sapiens (P55211)
brenda