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Human Caspase 9 Protein expressed in Escherichia coli (E. coli) - ABIN2487277
Azuma, Koths, Flanagan, Kwiatkowski: Gelsolin in complex with phosphatidylinositol 4,5-bisphosphate inhibits caspase-3 and -9 to retard apoptotic progression. in The Journal of biological chemistry 2000
Show all 8 Pubmed References
Inhibition of caspase-9 aggravates acute liver injury through suppression of cytoprotective autophagy.
inducible caspase-9 (iC9) safety switch can eliminate CD19.CAR-Ts in a dose-dependent manner, allowing either a selective containment of CD19.CAR-T expansion in case of CRS or complete deletion on demand granting normal B cell reconstitution.
Cepharanthine treatment reduced mitochondrial membrane potential and upregulated the level of cleaved caspases, including caspase-9 and caspase-3/7, in a dose-dependent fashion.
Bcl-2-caspase-9 apoptosis pathway was clearly activated in the testis of asthmatic mice with the increased expression of apoptosis-related proteins.
Inhibition of Caspase-9 restricted, while Apaf-1 promoted, Chlamydia pneumoniae infection in HEp-2, HeLa, and mouse epithelial fibroblast (MEF) cells.
The study demonstrates sublethal caspase-activation has an important role in cardiomyocyte differentiation and may have significant implications for promoting cardiac regeneration after myocardial injury involving exogenous or endogenous cell sources.
Casp6 knockout in YAC128 mice does not abolish the presence of the mutant HTT protein-586 fragment but ameliorates depression, body weight gain, IGF-1 and BDNF levels in YAC128 mice.
study demonstrates that MMP-3 leads to caspase-9 activation and suggests that this occurs indirectly via a cytosolic protein, possibly involving Apaf-1
caspase-9 mediates Puma activation to determine the threshold for overcoming chemoresistance in cancer cells.
Casp9, the initiator caspase of the intrinsic apoptotic cascade, has a role in murine fetal and adult hematopoiesis
Effect of cortisol on caspases in the co-cultured C2C12 and 3 T3-L1 cells.
findings demonstrate that focal activation of caspase-9 and -3 at neuromuscular junctions is essentially responsible for subsynaptic DNA damage and apoptotic synaptic degeneration in slow-channel myasthenic syndrome
The activity of caspase-3, -8 and -9 was significantly increased in the isoflurane-treated cells compared with the untreated cells.
After activation by caspase-9, caspase-3 inhibits ROS production and is required for efficient execution of apoptosis, while effector caspase-7 is required for apoptotic cell detachment.
The mitochondrial apoptotic pathway mediated by caspase 9 is constitutively activated in oocytes.
DP T cell apoptosis following experimental T. cruzi acute infection is dependent on glucocorticoid stimulation, promoting caspase-8 and -9 activation
caspase-9 activity is up-regulated by zVAD-fmk and is involved in an amplification loop of etoposide-induced cell death at the mitochondrial level in mouse embryonic fibroblasts.
Both megakaryocytes and platelets possess a functional apoptotic caspase cascade downstream of Bcl-2 family-mediated mitochondrial damage. Caspase-9 is the initiator caspase, and its loss blocks effector caspase activation.
Immunohistochemical expression of Bcl-2, p53 and caspase-9 in hypothalamus magnocellular centers of nNOS knockout mice following water deprivation
Results identify a cancer-specific mechanism of hnRNP L phosphorylation and subsequent lowering of the caspase-9a/9b ratio, which is required for the tumorigenic capacity of non-small cell lung cancer cells.
CASP9 mutations cause recurrent folate-resistant neural tube defects.
Study described rare mutations of the apoptosis gene CASP9 identified in neural tube defect cases and demonstrated that the p.Y251C variant impairs the protein's apoptotic function, suggesting it is a loss-of-function variation; also showed that the p.R191G variant inhibited apoptosis under folate-deficient condition, highlighting the effect of gene-environment interactions in this complex disease.
these results revealed that caspase9 and activated caspase3 predominantly regulates cell apoptosis in human dental pulp stem cells from deciduous teeth.
Low CASP9 expression is associated with Colorectal Cancer.
the results of the present study suggest that miR-96-5p, which is frequently upregulated in hepatocellular carcinoma (HCC), inhibits apoptosis by targeting CASP9. Therefore, miR-96-5p may be a potential therapeutic target for HCC
CASP9 germline mutations may have played a role at least in part to the susceptibility of development of gliomas in a Li-Fraumeni-like family lacking a TP53 germline mutation.
The caspase 9 level was significantly lower and related with oxidant status in patients with polycystic ovary syndrome, while the circulating levels of caspases 3 and 7 were statistically similar in both PCOS and control groups.
Results indicate that the apoptotic protease-activating factor 1 (Apaf-1) apoptosome activates caspase-9 in part through sequestration of the inhibitory caspase recruitment domains (CARDs) domain.
1,4-BQ evidently induced mitochondria-mediated apoptosis and increased pro-apoptotic genes (Caspase-9 and Caspase-3) expression in a dose-dependent manner.
DES1 plays a key role in palmitic acid-mediated caspase 9 and caspase 3 activation.
CASP9 expression associated with inhibition of miR-182.
CASP-9 polymorphism is associated with Primary Brain Tumors.
Fisetin inhibited Triple-Negative Breast Cancer Cells cell division and induced apoptosis, which was associated with mitochondrial membrane permeabilization and the activation of caspase-9 and caspase-8, as well as the cleavage of poly(ADP-ribose) polymerase-1.
High CASP9 expression is associated with Lung Tumorigenesis.
caspase-8 and caspase-9 contribute to the cyclic stretch-induced apoptosis, but functioned differently at different stages in human periodontal ligament cells
knockdown of HMGI-C led to the significant induction of apoptosis via mitochondrial pathway by inducing miR34a and cell cycle arrest in MDA-MB-468 cells in vitro.
Results suggest that the formation of the apoptosome accompanied by the activation of caspase-9 may occur in brains affected by multiple system atrophy (MSA), and that a mitochondria-dependent apoptotic pathway may be partially associated with the pathogenesis of MSA.
Using recombinant proteins, this study investigated the influence of survivin on the inhibition of caspase-9 by XIAP in vitro. With a fluorescence-based assay for the apoptosome-stimulated activity of caspase-9, the study shows that survivin has no effect on the inhibition of caspase-9 by XIAP, neither in the presence nor in the absence of Smac.
LRRC8A is an essential regulator of cisplatin induced p53 protein activity and its downstream signaling involving increased expression of p21Waf1/Cip1 and MDM2, as well as activation of caspase-9 and -3 in tumor cell lines.
Data show that caspase 9 (CASP9) single nucleotide polymorphism (rs1052576) TT genotype was seemed to be associated with higher risk of pathological stage.
Suppression of caspase-9 resulted in significant upregulation of cell proliferation-, adhesion-, growth-, development- and division-regulating genes, and the downregulation of cell death program- and stress response-regulating genes.
Endothelial cell apoptosis by H. somnus-activated platelets required activation of both caspase-8 and caspase-9.
Clonidine administration prior to hypoxia prevents the hypoxia-induced increase in the activity of caspases in the cerebral cortex.
The ATP and cytochrome c dependent activation of caspase-9 is increased during hypoxia. The ATP and cytochrome c sites of Apaf-1 that mediate caspase-9 activation are modified during hypoxia.
Results suggest that zearalenone induces apoptosis and necrosis of porcine granulosa cells in a dose-dependent manner via a caspase-3- and caspase-9-dependent mitochondrial pathway.
We conclude that the hypoxia-induced activation of caspase-9 is mediated by Src kinase.
This gene encodes a member of the cysteine-aspartic acid protease (caspase) family. Sequential activation of caspases plays a central role in the execution-phase of cell apoptosis. Caspases exist as inactive proenzymes which undergo proteolytic processing at conserved aspartic residues to produce two subunits, large and small, that dimerize to form the active enzyme. This protein is processed by caspase APAF1\; this step is thought to be one of the earliest in the caspase activation cascade. Alternative splicing results in two transcript variants which encode different isoforms.
, ICE-like apoptotic protease 6
, apoptotic protease Mch-6
, apoptotic protease-activating factor 3
, 25 kDa caspase-9 dominant negative protein
, Ice-like apoptotic protease 6
, apoptotic protease activating factor 3
, caspase-9 dominant negative form
, caspase-9-carboxyl-terminal divergent
, apoptotic protease MCH-6
, protein phosphatase 1, regulatory subunit 56
, caspase 9, apoptosis-related cysteine protease