Browse our anti-Caspase 9 (CASP9) Antibodies

Mouse (Murine) Caspase 9, Apoptosis-Related Cysteine Peptidase (CASP9) interaction partners

1. Apoptosis induced by ESAT-6 was mainly via the intrinsic pathway with elevated protein levels of cleaved caspase-9 and -3. Furthermore, ESAT-6 also induced Bim activation during this process.

2. Inhibition of caspase-9 aggravates acute liver injury through suppression of cytoprotective autophagy.

3. 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.

4. 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.

5. Bcl-2-caspase-9 apoptosis pathway was clearly activated in the testis of asthmatic mice with the increased expression of apoptosis-related proteins.

6. Inhibition of Caspase-9 restricted, while Apaf-1 promoted, Chlamydia pneumoniae infection in HEp-2, HeLa, and mouse epithelial fibroblast (MEF) cells.

7. 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.

8. 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.

9. study demonstrates that MMP-3 leads to caspase-9 activation and suggests that this occurs indirectly via a cytosolic protein, possibly involving Apaf-1

10. caspase-9 mediates Puma activation to determine the threshold for overcoming chemoresistance in cancer cells.

11. Casp9, the initiator caspase of the intrinsic apoptotic cascade, has a role in murine fetal and adult hematopoiesis

12. Effect of cortisol on caspases in the co-cultured C2C12 and 3 T3-L1 cells.

13. 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

14. The activity of caspase-3, -8 and -9 was significantly increased in the isoflurane-treated cells compared with the untreated cells.

15. 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.

16. The mitochondrial apoptotic pathway mediated by caspase 9 is constitutively activated in oocytes.

17. DP T cell apoptosis following experimental T. cruzi acute infection is dependent on glucocorticoid stimulation, promoting caspase-8 and -9 activation

18. 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.

19. 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.

20. Immunohistochemical expression of Bcl-2, p53 and caspase-9 in hypothalamus magnocellular centers of nNOS knockout mice following water deprivation

Human Caspase 9, Apoptosis-Related Cysteine Peptidase (CASP9) interaction partners

1. the present study showed that lncRNA POU3F3 may promote proliferation and inhibit apoptosis of cancer cells in triple-negative breast cancer by inactivating caspase 9.

2. Compared with GG genotype carriers, AA genotype carriers had a statistically significant difference in the expression of caspase-9 in nucleus pulposus. There was no correlation between the MRI score of lumbar disc degeneration and the expression of caspase-9 in the degenerated nucleus pulposus.

3. Results strongly suggest that rare mutations in apoptosis-related genes including CASP9, APAF1, and CASP3 contribute to etiology of neural tube defects in Han Chinese population.

4. Serum CASP9 levels were significantly lower in the patients group than in the control group (p<0.0001). CASP9 Ex5+32 GG genotype was a risk factor whereas the variant A allele could be a risk-reducing factor for Non-small cell lung cancer .

5. Gallium complexes significantly depleted cellular iron, resulting in upregulation of transferrin receptor-1 and downregulation of ferritin. They also effectively activate the caspase family proteins (caspase-3/7/9), promote the release of cytochromes from the mitochondria, and ultimately lead to apoptosis.

6. Inhibition of TRIAP1 in RPMI8226 cells increased the percentage of apoptotic cells, accompanied by increased expression of APAF1 and Caspase 9, and Caspase 9 and Caspase 3/7 activity.

7. This effect was mediated by an increase in the expression of genes encoding p21, p27, caspase 3, caspase 9 as well a decrease in transcription of AKT1 and S6K1.

8. Mechanistic insights into a new level of caspase-9 regulation, prompting speculation that the CARD may also play a role in the recruitment or recognition of substrate.

9. CASP9 mutations cause recurrent folate-resistant neural tube defects.

10. 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.

11. these results revealed that caspase9 and activated caspase3 predominantly regulates cell apoptosis in human dental pulp stem cells from deciduous teeth.

12. Low CASP9 expression is associated with Colorectal Cancer.

13. 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

14. 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.

15. 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.

16. 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.

17. 1,4-BQ evidently induced mitochondria-mediated apoptosis and increased pro-apoptotic genes (Caspase-9 and Caspase-3) expression in a dose-dependent manner.

18. DES1 plays a key role in palmitic acid-mediated caspase 9 and caspase 3 activation.

19. CASP9 expression associated with inhibition of miR-182.

20. CASP-9 polymorphism is associated with Primary Brain Tumors.

Cow (Bovine) Caspase 9, Apoptosis-Related Cysteine Peptidase (CASP9) interaction partners

1. 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.

2. Endothelial cell apoptosis by H. somnus-activated platelets required activation of both caspase-8 and caspase-9.

Pig (Porcine) Caspase 9, Apoptosis-Related Cysteine Peptidase (CASP9) interaction partners

1. Clonidine administration prior to hypoxia prevents the hypoxia-induced increase in the activity of caspases in the cerebral cortex.

2. 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.

3. 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.

4. We conclude that the hypoxia-induced activation of caspase-9 is mediated by Src kinase.