Young Sik Cho

TL;DR: The findings suggest that RIP3 controls programmed necrosis by initiating the pronecrotic kinase cascade, and that this is necessary for the inflammatory response against virus infections.

TL;DR: It is found that mutation of individual serine residues in the kinase domain of RIP1 had little effect on RIP1 kinase activity and TNF-induced programmed necrosis, and an alanine residue substitution for Ser(89) enhanced RIP1-RIP3 necrosome formation, indicating that Ser( 89) is an inhibitory phosphoacceptor site that can dampen the pro-necrotic function of RIP 1.

TL;DR: Different adjuvants have different modes of action and a better understanding of their immunology could provide guidance for the development of novel adjuvant-based vaccines, according to this review.

TL;DR: The results reveal that besides RIP1, Nec-1 also targets other factors crucial for necrosis induction in L929 cells, and high doses of Nec- 1 inhibit other signal transduction pathways such as that for T cell receptor activation.

TL;DR: It is found that LCA caused apoptotic cell death in HSC4 and HN22 cells, as characterized by sub-G1 population, nuclear condensation, Annexin V staining, and multi-caspase activity and apoptotic regulatory proteins such as Bax, Bid, Bcl(-xl), caspase-3 and PARP.