Emad S. Alnemri

TL;DR: Evidence is provided that IL‐4 suppresses NLRP3‐dependent caspase‐1 activation and the subsequent IL‐1β secretion but does not inhibit absent in melanoma 2 (AIM2)‐ or NLRC4 (NOD‐like receptor family, CARD domain‐containing 4)‐ dependent casp enzyme activation in THP‐1 and mouse bone marrow‐derived macrophages, thus providing an endogenous regulatory machinery to prevent excessive inflammasome activation.

TL;DR: Data indicate for the first time that c-FLIPL might control germ cell apoptosis and caspase activity in the adult testis.

TL;DR: E1A is capable of activating caspase-8 by a Bcl-2-inhibitable pathway that does not involve autocrine stimulation of FADD-dependent death receptor pathways, and contrasts with the anti-apoptotic influence of B cl-2 family proteins in the cell death pathway induced by Fas ligand or tumor necrosis factor.

TL;DR: The observation that caspase-9 moves from mitochondria into the nucleus on the induction of apoptosis provides this caspases with a possible new role.

TL;DR: It is demonstrated that FGF2 treatment differentially regulates members of the tumor necrosis factor (TNF) superfamily of death domain receptors and their ligands and the observation that multiple trophic inputs are required for the survival of specific neurons is provided.