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Crosstalk in TNFR1 signaling. Ligation of TNFR1 leads to activation of the pro-inflammatory NF-κB and JNK, and pro-apoptotic caspase-8 and ROS pathways. However, in normal cells, NF-κB target gene products suppress pro-apoptotic pathways. For instance, cIAP1/2 and cFLIP inhibit caspase-8 activation, XIAP and GADD45β suppress prolonged JNK activation, and FHC and Mn-SOD inhibit ROS accumulation. Therefore, unless NF-κB pathway is blocked, TNFα is insufficient to induce cell death.
