EC Number |
General Information |
Reference |
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3.4.22.61 | malfunction |
in p62-deficient cancer cells caspase-8 activity and apoptosis are diminished, yet not abrogated |
717276 |
3.4.22.61 | malfunction |
loss of caspase 8 prevents CYLD degradation, resulting in necrotic death. Mutation of the caspase 8 processing site on the substrate converts a pro-survival response to necrotic death without the need for caspase 8 inhibition |
718144 |
3.4.22.61 | malfunction |
mice deficient in caspase-8 in basal epidermal keratinocytes suffer from chronic skin inflammation, as an apparent consequence of IRF3 hyper-activation. Catalytically active caspase-8 is required to rescue the lymphocyte development in caspase-8 deficient mice. The developmental phenotype observed in the caspase-8 knockout mouse is shared with both the FLIPL knockout and the FADD knockout |
717282 |
3.4.22.61 | malfunction |
no change in A-SMase activity in caspase-8-deficient cells. Retransfection of caspase-8-deficient Jurkat cells with an expression plasmid for caspase-8 restores the ability of the transfected cells to respond to TNF stimulation by increased A-SMase activity. Caspase-8-deficient Jurkat cells are almost completely resistant to TNF/CHX treatment |
717539 |
3.4.22.61 | malfunction |
proliferative defects of caspase 8-deficient T cells and B cells. Caspase-8 deficiency causes programmed necrotic cell death |
718154 |
3.4.22.61 | malfunction |
silencing of caspase 8 gene is a key factor controlling the outcome of neonatal astrocytes upon Fas engagement, restoration of caspase 8 expression triggers apoptotic cell death in primary neonatal astrocytes |
710108 |
3.4.22.61 | metabolism |
activation of caspase 8 is upstream of caspase 3 activation |
717470 |
3.4.22.61 | metabolism |
caspase-8 and Bid are the known procurers of the death signal leading from death receptor stimulation to permeabilisation of the outer mitochondrial membrane in the apoptotic pathway, regulation of caspase-8 and Bid function and activation, overview |
717276 |
3.4.22.61 | metabolism |
caspase-8 of the extrinsic pathway is able to activate upstream mediators of the intrinsic apoptotic pathway |
709367 |
3.4.22.61 | metabolism |
mathematical modeling of CD95 DISC-mediated MAPK activation and apoptosis, overview. Quantitative dynamics of DED proteins, procaspase-8, and c-FLIP, which lead to caspase-8 activation and induction of apoptotic and non-apoptotic signaling pathways |
717460 |