Kim Burns

TL;DR: The characterization of an inhibitor of apoptosis is reported, designated FLIP (for FLICE-inhibitory protein), which is predominantly expressed in muscle and lymphoid tissues and may be implicated in tissue homeostasis as an important regulator of apoptotic regulation.

TL;DR: A new family of viral inhibitors (v-FLIPs) which interfere with apoptosis signalled through death receptors3 and which are present in several γ-herpesviruses (including Kaposi's-sarcoma-associated human herpesvirus-8), as well as in the tumorigenic human molluscipoxvirus4.

TL;DR: This work investigated the 'downstream' signaling events that regulate TLR3-dependent Trif-induced NF-κB activation and found that RIP1 mediates Trif -RIP1–inducedNF-κBs activation.

TL;DR: It is shown that TRAil-R1 can associate with TRAIL-R2, suggesting that TRAIL may signal through heteroreceptor signaling complexes, and can signal both death and gene transcription, functions reminiscent of those of TNFR1 and TRAMP.

TL;DR: Evidence is provided that FLIP is not simply an inhibitor of death-receptor-induced apoptosis but that it also mediates the activation of NF-kappaB and Erk by virtue of its capacity to recruit adaptor proteins involved in these signaling pathways.