BNIP3 regulates mitophagy and apoptosis in delayed neuronal death in stroke

BNIP3 upregulation and EndoG translocation in delayed neuronal death in stroke and in hypoxia.

BACKGROUND AND PURPOSE Delayed neuronal death is a hallmark feature of stroke and the primary target of neuroprotective strategies. Caspase-independent apoptosis pathways are suggested as a mechanism for the delayed neuronal injury. Here we test the hypothesis that one of the caspase-independent apoptosis pathways is activated by BNIP3 and mediated by EndoG. METHODS We performed immunohistoch...

Neuronal Mitophagy in Neurodegenerative Diseases

Neuronal homeostasis depends on the proper functioning of different quality control systems. All intracellular components are subjected to continuous turnover through the coordinated synthesis, degradation and recycling of their constituent elements. Autophagy is the catabolic mechanism by which intracellular cytosolic components, including proteins, organelles, aggregates and any other intrace...

Apoptosis: neuronal death by design.

182 J Clin Psychiatry 58:5, May 1997 ying is generally an undesired affair. In recent years, however, it has become clear that many cells, including neurons, are actively programmed to commit molecular hari-kari. Such a process is called apoptosis. This is not the messy affair associated with cellular poisoning or suffocation, known as necrosis. Necrotic cell death is characterized by a severe ...

Modulation of serines 17 and 24 in the LC3-interacting region of Bnip3 determines pro-survival mitophagy versus apoptosis.

BH3-only proteins integrate apoptosis and autophagy pathways, yet regulation and functional consequences of pathway cross-talk are not fully resolved. The BH3-only protein Bnip3 is an autophagy receptor that signals autophagic degradation of mitochondria (mitophagy) via interaction of its LC3-interacting region (LIR) with Atg8 proteins. Here we report that phosphorylation of serine residues 17 ...

Apoptosis-Inducing Factor Regulates Death