Monitoring Autophagy in Neurons

Lysosomal Dysfunction is Linked to Exosomal Secretion

Autophagy independent roles of the core ATG proteins

Nuclear LC3: Why is it there and what is it doing?

Cross-talk between proteasome degradation and lysosomal degradation

Brain size matters: MTOR regulates autophagy and number of cortical interneurons

From Then ‘till Now: The History of Autophagy and Cancer Research

The Proteasome and Autophagy Pathways in Alzheimer's Disease

The neurodegenerative disorder, Alzheimer's disease, is responsible for 60 to 80% of all dementia cases.1   Neurodegeneration occurs in response to the accumulation of amyloid-β plaques and neurofibrillary tangles composed of hyperphosphorylated tau.

Application guide: Methods to monitor Autophagy

Autophagy is an essential process that cells utilize to degrade and recycle damaged material and fuel metabolism, especially under stress.  The process is evolutionarily conserved and complex, relying on over 20 key proteins. Induction of autophagy is mediated by the formation of the ULK and BECLIN complexes, the latter of which includes BH3-containing proteins and AMBRA1, resulting in the formation of a double membrane phagophore structure.

Key Targets in Apoptosis, Necroptosis, and Autophagy

Cell death/recycling pathways such as apoptosis, necroptosis, and autophagy are an integral part of the growth, development, homeostasis as well as the pathophysiology in the life of living organisms. These signaling pathways are highly regulated and some of their key regulatory targets are discussed below.


Apoptosis, programmed cell death, is primarily characterized by the activation of caspases which further regulate the mass cleavage of proteins and DNA. Some of major the proteins responsible for various apoptotic events are: