Liora Lindenboim

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Autophagy, a cellular degradation system, promotes both cell death and survival. The interaction between Bcl-2 family proteins and Beclin 1, a Bcl-2 interacting protein that promotes autophagy, can mediate crosstalk between autophagy and apoptosis. We investigated the interaction between anti-and pro-apoptotic Bcl-2 proteins with Beclin 1. Our results show(More)
Bcl-xL, a member of the bcl-2 family of proteins is required for the survival of neurons early in development. To study the mechanism of action of Bcl-xL in a neuronal context, we generated rat PC12 cells overexpressing Bcl-xL and examined their susceptibility to apoptotic stimuli that induce apoptosis through different pathways involving trophic-factor(More)
Apoptosis is regulated by the action of the Bcl-2 family of proteins, which includes anti- and pro-apoptotic members such as Bcl-xS and Bax. These proteins may differ from each other in structure, mechanism of action and interactions with anti-apoptotic signaling. The mechanism whereby Bax induces cell death has been studied in some cellular systems, but(More)
Previous studies have shown that PC12 cells depend on growth factors for their survival. When deprived of growth factors, the cells undergo a dying process termed "apoptosis" (programed cell death). We show here that muscarinic agonists inhibited the apoptotic death of growth factor-deprived PC12M1 cells (PC12 cells stably expressing cloned m1 muscarinic(More)
An important mechanism in apoptotic regulation is changes in the subcellular distribution of pro- and anti-apoptotic proteins. Among the proteins that change in their localization and may promote apoptosis are nuclear proteins. Several of these nuclear proteins such as p53, Nur77, histone H1.2, and nucleophosmin were reported to accumulate in the cytosol(More)
Pheochromocytoma (PC12) cells have been shown to undergo apoptosis (programmed cell death) when deprived of serum and to be rescued by nerve growth factor, fibroblast growth factor, dibutyryl cyclic AMP, aurintricarboxylic acid, or exogenous expression of bcl-2. We show here that the cytotoxic drugs cycloheximide, actinomycin D, colchicine, and EGTA also(More)
Bcl-x(S), a pro-apoptotic member of the Bcl-2 protein family, is localized in the mitochondrial outer membrane and induces caspase-dependent and nerve growth factor (NGF)-inhibitable apoptosis in PC12 cells. The mechanism of action of Bcl-x(S) and how NGF inhibits this death are not fully understood. It is still unknown whether Bcl-x(S) induces(More)
Previous studies have shown that caspases (proteases related to interleukin-1beta converting enzyme) are needed for the death of trophic factor-deprived PC12 cells. However, the protease involved in this process has not been identified. The results presented here strongly suggest that caspase-2 (Nedd2/Ich-1) plays a major role in the death of serum-deprived(More)
Previous studies have shown that PC12 cells undergo apoptosis (programmed cell death) when deprived of serum. In the present study, we examined the relationship of this death process to the cell cycle. PC12 cell populations synchronized at different, specific phases of the cell cycle exhibit similar kinetics of cell death following deprivation of serum.(More)
The mechanism of action of pro-apoptotic proteins is difficult to study in vivo because of their death effect, which makes it problematic to obtain sufficient homogeneous experimental material for biochemical analysis. We show here that pro-apoptotic genes expressed in Xenopus oocytes constitute a useful in vivo system for studying their mechanism of(More)