Figure 22

Receptor interacting protein (RIP) kinase 1 as a crucial cellular crossroads affecting whether target cells survive or die. ROS may increase in the cells also as a consequence of increased release by mithocondria, as in the case of TNFα and FasL-related responses. Activation of death receptor (DR), Toll-like receptors (TLRs) as well as signalling pathways initiated upon detection of intracellular stress (including oxidative stress itself and/or DNA damage) all have been reported to converge on RIP, particularly RIP1; the cellular context will then drive the RIP-related response of target cells towards survival by preferentially inducing activation of NF-κB and/or MAPK, or to cell death by inducing either true apoptosis or a form of caspase-independent cell death [193], although this is an oversimplified scheme (for example, sustained JNK activation is a well known event leading to cell death).