Browse our anti-Caspase 8 (CASP8) Antibodies

Xenopus laevis Caspase 8, Apoptosis-Related Cysteine Peptidase (CASP8) interaction partners

1. Furthermore, while activities to process procaspase-8 and procaspase-9 appeared in SAMDC-overexpressed apoptotic embryos, the activity to process procaspase-8 did not appear in p53-overexpressed apoptotic embryos.

2. tail regression at metamorphosis implicates an apoptotic pathway inducible by T(3) hormone in an organ autonomous manner and involving the cell death executioners BH3 interacting domain death agonist and Caspases-2 and -8

Mouse (Murine) Caspase 8, Apoptosis-Related Cysteine Peptidase (CASP8) interaction partners

1. TLR stimulation led to IRAKM-caspase-8-ASC complex formation, resulting in the activation of caspase-8 and IL-1beta release in microglia.

2. These findings indicate that the triggering of inflammation by Casp8 deletion in mice occurs, in part, independently of necroptosis or other functions of RIPK3, and rather reflects enhanced RIPK1-dependent signaling for activation of inflammatory genes.

3. Casp8 signaling is dispensable to the generation of immunity against herpesvirus infection

4. Polo-like kinase 1 is recruited into mitotic ripoptosomes, where PLK1's activity is controlled via RIPK1-dependent recruitment and Caspase-8-mediated cleavage, ensuring chromosome stability and faithful chromosome segregation during mitosis.

5. caspase-8 acts as a regulator of GSDMD-driven cell death.

6. AIM2 inflammasome activates caspase-1 independent of caspase-8. Caspase-1 and caspase-8 are both upstream of caspase-3 cleavage initiated by AIM2.

7. Pro-apoptotic caspase-8 has to be present with pro-pyroptotic caspase-11 to support tumor necrosis factor- and interferon-beta-dependent tissue injury first observed in the small intestine and later in spleen and thymus. Combined pyroptotic and apoptotic signaling mediated endotoxemia independently of RIPK1 kinase activity and RIPK3 function.

8. Results uncover a form of caspase-8-mediated pyroptosis and suggest a hypothesis for the increased sensitivity of humans to Yersinia infection compared with the rodent reservoir.

9. these results demonstrate that Caspase-8 is essential to prevent Salmonella Typhimurium induced enteritis and to ensure host survival

10. These data demonstrate that caspase-8 functions in synovial antigen-presenting cells to regulate the response to inflammatory stimuli by controlling RIPK3 action, and this delicate balance maintains homeostasis within the joint.

11. Results illustrate the temporal and spatial activation of caspase-8 and -3 in microglia/macrophages occurring upon ischemic stroke and suggest that the expression of these caspases could be used in neuropathological diagnostic work.

12. Caspases and their substrates are key mediators of apoptosis.

13. inhibition of TAK1 triggered two caspase 8 activation pathways through the induction of RIP1-FADD-caspase 8 complex as well as FLIP cleavage/degradation.

14. this study identifies a crucial role for caspase-8 in the development of allergic airway inflammation

15. Prolonged treatment of human PMNs or mice bone marrow derived neutrophils (BMDN) with nitric oxide led to enhanced reactive oxygen species generation, caspase-8/caspase-3 cleavage, reduced mitochondrial membrane potential and finally cellular apoptosis.

16. caspase-8-dependent apoptosis was linked to hepatocellular carcinoma development.

17. Statistically significant increases in the expression of Fas and caspase-8 were observed, along with other molecules involved in the extrinsic apoptotic pathway such as Dapk1, Traf3, Tnsf12, Tnfrsf1A and Ripk1.

18. Results suggest that caspase-8 could regulate receptor-interacting protein 3 (RIP3)-mediated necroptosis.

19. we show that caspase-8 activity promotes cell-intrinsic cytokine expression, independent of its role in cell death in response to Yersinia infection

20. Data indicate that NLRC4 activation in Intestinal epithelial cells (IECs) leads to cell expulsion and IL-18 release, and implicate Caspase-8 in NLRC4 inflammasome responses in vivo by generation of doubly deficient in Caspase-1 and Caspase-8.

Human Caspase 8, Apoptosis-Related Cysteine Peptidase (CASP8) interaction partners

1. Structural basis for dimerization of the death effector domain of the F122A mutant of Caspase-8

2. REVIEW: recent data on the mechanisms of activating initiator caspase-8 in DED filaments are considered that allow us to better understand the subtle mechanisms of the initiation of the programmed cell death

3. Elevated levels of FADD and caspase-8, but not caspase-3, are associated with increased incidence of ischemic stroke.

4. elevated high expression of CASP3 or CASP8 in the neurons from MPs was accompanied by a decreased expression of GAL. To our knowledge, this is the first report describing the decomposition of myenteric plexuses (MPs) within cancer-affected human stomach wall and the possible role of apoptosis in this process

5. Caspase-8 rs3834129 genotypes play a minor role in the personal susceptibility to bladder cancer in Taiwan.

6. zinc finger protein 91 positively regulates the production of IL-1beta in macrophages by activation of MAPKs and non-canonical caspase-8 inflammasome

7. TLR stimulation led to IRAKM-caspase-8-ASC complex formation, resulting in the activation of caspase-8 and IL-1beta release in microglia.

8. both caspase-8-dependent and -independent apoptotic mechanisms are activated in triple-negative breast cancer cells undergoing sustained endoplasmic reticulum stress.

9. Evidence was provided within a moderate and representative population showing that caspase-8 rs3834129 was not associated with increased colorectal cancer (CRC) risk in a Taiwanese population.

10. Polo-like kinase 1 is recruited into mitotic ripoptosomes, where PLK1's activity is controlled via RIPK1-dependent recruitment and Caspase-8-mediated cleavage, ensuring chromosome stability and faithful chromosome segregation during mitosis.

11. No significant difference was observed in genotypic or allelic frequencies between control and endometriosis groups for rs13416436 and rs2037815 (CASP8 gene). On the other hand, a significant difference between rs3740286 and rs4064 (FAS gene) was found. Regarding polymorphisms in the FAS gene, a statistically significant difference was found in co-dominant and dominant models.

12. CASP8 deficiency is a novel cause of very early onset-inflammatory bowel disease associated with lymphocyte dysfunction, impaired inflammasome activation, and defec- tive epithelial cell death responses.

13. Data show that ionizing radiation (IR) induces apoptosis in THP-1 cells through cas-8-mediated pathways, whereas THP-1-derived macrophages (THP-1-M) are resistant to IR due to impaired casp-8-mediated apoptosis during differentiation and not to a capacity for DSB repair suggesting that the regulation of casp-8-mediated apoptosis during differentiation plays a role in the p53-independent radio-resistance of THP-1-M.

14. The apoptosis was partially dependent upon caspase-8 concomitant with attenuated NF-kappa B survival signal due to stimulus of TNF-alpha. It suggests that PAK4 as target is a switch between caspase-8 apoptosis and NF-kappa B survival signals induced by TNF-alpha in hepatocarcinoma cells.

15. The caspase 8 mediated RIPK1 cleavage product has a pro-apoptotic function, and further cleavage of this pro-apoptotic cleavage product by human rhinovirus 3C protease may provide a mechanism by which human rhinovirus limits apoptosis.

16. results suggest that miR-21 regulates the apoptosis of keloid fibroblasts via targeting FasL, and caspase-8 and the mitochondria-mediated apoptotic signaling pathway is involved in this process.

17. Caspase-3 and -8 and annexin V may serve as diagnostic markers in Ovarian cancer , also explained that the decrement in control of the S phase in the cell cycle may considered one of the significant factors in the development of ovarian tumors

18. neither rs13416436 nor rs2037815 associated with pre-eclampsia

19. High CASP8 expression is associated with Colorectal Cancer.

20. Sleep duration is associated with plasma caspase-8. Caspase-8 independently predicts diabetes mellitus years before disease onset and modifies the effect of sleep duration on incident diabetes mellitus.

Cow (Bovine) Caspase 8, Apoptosis-Related Cysteine Peptidase (CASP8) interaction partners

1. S. aureus-induced apoptosis in bovine mammary epithelial cells apoptosis was mitigated by caspase-3 and caspase-8 inhibitors, suggesting that apoptosis is initiated via caspase-8 activation.

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

Pig (Porcine) Caspase 8, Apoptosis-Related Cysteine Peptidase (CASP8) interaction partners

1. mmediately after hypoxia C8 and C1 follow a similar pattern of increase while long term this appears to dissociate

2. induces apoptosis in porcine ovarian follicles

3. Nitric oxide-dependent increase in caspase-8 mRNA levels is associated with phosphorylation of STAT-1 at Ser-727 and STAT1 binding to the caspase-8 promoter in cultured lung endothelial cells.

4. Data show that cysteine significantly reduced the expression of pro-inflammatory cytokines, including TNF-alpha, IL-6, IL-12p40, IL-1beta, and resulted in increased expression of the apoptosis initiator caspase-8 and bcl2L1.

Zebrafish Caspase 8, Apoptosis-Related Cysteine Peptidase (CASP8) interaction partners

1. Induction of apoptosis through targeted activation of caspase by tamoxifen (ATTAC(TM)) further expands the repertoire of genetic tools for conditional interrogation of cellular functions.

2. Targeted gene knockdown of TNFRSF1B in zebrafish embryos results in the induction of a caspase-8, caspase-2 and P53-dependent apoptotic program in endothelial cells that bypasses caspase-3.

3. These results show that zebrafish casp8 has a structure and function similar to mammalian CASP8 orthologs and the role of caspase-8 in the apoptotic signal pathway has been conserved over at least 450 million years of vertebrate evolution.