The goal of this project is to define how basic cellular mechanisms suppress, activate and execute the process of apoptosis or programmed cell death. Apoptosis is a fundamental component of virtually all aspects of biology, being critical for both developmental and cellular homeostasis in all multi-cellular organisms. Extensive studies worldwide have now implicated either excess or impaired apoptosis in numerous human diseases including cancer, AIDS, autoimmune diseases, sepsis, as well as toxic responses to environmental agents. Additionally, many of the therapies used for the treatment of cancer work by the activation of inherent cellular apoptotic programs.
|Franco, Rodrigo; Bortner, Carl D; Schmitz, Ingo et al. (2014) Glutathione depletion regulates both extrinsic and intrinsic apoptotic signaling cascades independent from multidrug resistance protein 1. Apoptosis 19:117-34|
|Galluzzi, L; Aaronson, S A; Abrams, J et al. (2009) Guidelines for the use and interpretation of assays for monitoring cell death in higher eukaryotes. Cell Death Differ 16:1093-107|
|Bortner, Carl D; Sifre, Maria I; Cidlowski, John A (2008) Cationic gradient reversal and cytoskeleton-independent volume regulatory pathways define an early stage of apoptosis. J Biol Chem 283:7219-29|
|Franco, Rodrigo; DeHaven, Wayne I; Sifre, Maria I et al. (2008) Glutathione depletion and disruption of intracellular ionic homeostasis regulate lymphoid cell apoptosis. J Biol Chem 283:36071-87|
|Ajiro, Kozo; Bortner, Carl D; Westmoreland, Jim et al. (2008) An endogenous calcium-dependent, caspase-independent intranuclear degradation pathway in thymocyte nuclei: antagonism by physiological concentrations of K(+) ions. Exp Cell Res 314:1237-49|