EC Number   |
Specific Activity Minimum [µmol/min/mg] |
Specific Activity Maximum [µmol/min/mg] |
Reference  |
|---|
   3.4.22.62 | -999 |
- |
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 |
695657 |
| 3.4.22.62 | -999 |
- |
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 |
695934 |
| 3.4.22.62 | -999 |
- |
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 |
696132 |
| 3.4.22.62 | -999 |
- |
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 |
696561 |
| 3.4.22.62 | -999 |
- |
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 |
697082 |
| 3.4.22.62 | -999 |
- |
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 |
697116 |
| 3.4.22.62 | -999 |
- |
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 |
697186 |
| 3.4.22.62 | -999 |
- |
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 |
697538 |
| 3.4.22.62 | -999 |
- |
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 |
697541 |
| 3.4.22.62 | -999 |
- |
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 |
697784 |
