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
-
3.4.22.62
-
caspase-3
-
bcl-2
-
parp
-
anti-apoptotic
-
pro-apoptotic
-
tunel
-
necrosis
-
apoptosis-related
-
caspase-dependent
-
apoptosis-inducing
-
jnk
-
apaf-1
-
annexin
-
extrinsic
-
cyclin
-
leukemia
-
bid
-
neuroprotective
-
depolarization
-
polyadp-ribose
-
survivin
-
hoechst
-
z-vad-fmk
-
antiproliferative
-
adp-ribose
-
xiap
-
iodide
-
deoxynucleotidyl
-
mitochondria-dependent
-
mitochondria-mediated
-
cisplatin
-
dutp
-
fadd
-
procaspase-3
-
caspase-mediated
-
pan-caspase
-
fas-mediated
-
trail
-
fas-associated
-
trail-induced
-
bcl-2-associated
-
apoptogenic
-
pharmacology
-
cdc25c
-
puma
-
transferase-mediated
-
executioner
-
factor-related
-
deltapsim
-
medicine
-
tunel-positive
-
sub-g1
- 3.4.22.62
- caspase-3
- bcl-2
- parp
-
anti-apoptotic
-
pro-apoptotic
-
tunel
- necrosis
-
apoptosis-related
-
caspase-dependent
-
apoptosis-inducing
- jnk
- apaf-1
-
annexin
-
extrinsic
- cyclin
- leukemia
- bid
-
neuroprotective
-
depolarization
-
polyadp-ribose
- survivin
-
hoechst
- z-vad-fmk
-
antiproliferative
- adp-ribose
- xiap
- iodide
-
deoxynucleotidyl
-
mitochondria-dependent
-
mitochondria-mediated
- cisplatin
- dutp
- fadd
- procaspase-3
-
caspase-mediated
-
pan-caspase
-
fas-mediated
-
trail
-
fas-associated
-
trail-induced
-
bcl-2-associated
-
apoptogenic
- pharmacology
- cdc25c
- puma
-
transferase-mediated
-
executioner
-
factor-related
-
deltapsim
- medicine
-
tunel-positive
-
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
Advanced search results
Specific Activity
Specific Activity on EC 3.4.22.62 - caspase-9
Please wait a moment until all data is loaded. This message will disappear when all data is loaded.
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
-
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
-
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
-
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
-
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
-
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
-
the poly-L-glutamic acid (PGA) derivative PGA-1 is capable of reducing hypoxia-induced apoptosis in primary culture cardiomyocytes
additional information
-
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