Yutaka Shimizu

TL;DR: It is shown that both constitutive and Tie2-Cre-driven HOIP deletion lead to aberrant endothelial cell death, resulting in defective vascularization and embryonic lethality at midgestation, and that HOIP's catalytic activity is necessary for preventing TNF-induced cell death.

TL;DR: The results demonstrate that both HOIP and HOIL-1 are essential LUBAC components and are required for embryogenesis by preventing aberrant cell death and reveal that when LUBac and caspase-8 are absent, RIPK3 prevents RIPK1 from inducing embryonic lethality by causing defects in fetal haematopoiesis.

TL;DR: The current knowledge on linear ubiquitination in immune signaling pathways and the biochemical mechanisms as to how linear polyubiquitin exerts its functions distinctly from those of other ubiquitin linkage types are reviewed.

TL;DR: This work mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage through DNA damage-sensing mechanism in hepatocytes.

TL;DR: It is shown that LUBAC forms part of the TRAil‐R‐associated complex I as well as of the cytoplasmic TRAIL‐induced complex II, which controls the TRAIL signalling outcome from complex I and II, two platforms which both trigger cell death and gene activation.