Robert W. Marquis

TL;DR: Two small molecule RIP3 kinase inhibitors are described and employ them to demonstrate the common requirement for RIP3 Kinase in programmed necrosis induced by RIP1-RIP3, DAI- RIP3, and TRIF-RIP 3 complexes.

TL;DR: It is demonstrated that the full four-helical bundle domain (4HBD) in the N-terminal region of MLKL is required and sufficient to induce its oligomerization and trigger cell death, and found that a patch of positively charged amino acids on the surface of the 4HBD binds to phosphatidylinositol phosphates (PIPs) and allows recruitment ofMLKL to the plasma membrane.

TL;DR: This work highlights a common mechanism unveiling RHIM-driven apoptosis by therapeutic or genetic perturbation of RIP3, which holds both necroptosis and apoptosis in balance through a Ripoptosome-like platform.

TL;DR: Novel, non-thiazolidinedione agonists for PPARγ and PPARδ that were identified by radioligand binding assays improve hyperglycemia and hypertriglyceridemia in vivo and are able to potentiate preadipocyte differentiation.

TL;DR: A linking strategy to synergize the effect of two symmetry-related amidobenzimidazole-based compounds to create linked ABZIs (diABZIs) with enhanced binding to STING and cellular function is developed, representing a milestone in the rapidly growing field of immune-modifying cancer therapies.