As we know, the death ligands like TNF-alpha or TRAIL trigger apoptosis only when inhibitors of gene transcription or protein synthesis is supplemented as the death receptors normally activate two arms of reaction on ligation; they induce apoptosis and activate an anti-apoptotic transcription factor, NFkappaB. The later arm of reaction initiates the transcription of a panel of anti-apoptotic factors. Only when the synthesis of apoptotic inhibitor is blocked by such reagents like cycloheximide or actinomycin D, apoptosis would be efficiently induced. In fact, the cytokine induced apoptosis is executed very rapidly; the blebbing cells are visible within two hours after the treatment. This is the case for TNFR1 or TRAILRs (DR4 and DR5) mediated apoptosis. If FAS ligand is supplemented to the medium, some says that the manipulation fail to induce apoptosis, but one should use the IgM type agonistic anti-FAS antibody CH11. The question is, does the antibody alone trigger FAS-mediated apoptosis in susceptible cells?
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