Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Posttranslational Modification | Comment | Organism |
---|---|---|
proteolytic modification | CD95 DISC-induced caspase-8 activity, mechanism, the long c-FLIP isoform, c-FLIPL, and the short c-FLIP isoform, c-FLIPR, inhibit caspase-8 processing at the DISC | Homo sapiens |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
HeLa cell | - |
Homo sapiens | - |
General Information | Comment | Organism |
---|---|---|
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 | Homo sapiens |
physiological function | caspase-8 activity has an essential role in CD95/Fas-mediated MAPK activation. Stimulation of CD95/Fas/APO-1 results in the induction of both apoptotic and non-apoptotic signaling pathways. CD95 DISC-induced caspase-8 activity is important for the initiation of ERK1/2 and p38 MAPK activation, caspase-8 activation mechanism, overview. The long c-FLIP isoform, c-FLIPL, and the short c-FLIP isoform, c-FLIPR, inhibit MAPK induction by blocking caspase-8 processing at the DISC. Caspase-8 activity is also essential to MAPK activation in response to anti-APO-1 stimulation | Homo sapiens |