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:

The use of the autophagy marker LC3 in western blot, immunocytochemistry and flow cytometry research applications as an indicator of autophagy

The process of autophagy, or lysosome-mediated degradation of damaged proteins and organelles in the cytosol, is a vital cellular process that acts as a quality control mechanism for proteins and organelles. The misregulation of autophagy can lead to an imbalance of cellular homeostasis and the subsequent development of disease.  Therefore, the study of autophagy is at the forefront of neuroscience and cancer research, among others.

Required proteins for p62/SQSTM1 regulation and a role for p62/SQSTM1 in neuronal autophagy

Autophagy is a crucial cellular process that clears the cell of protein aggregates, toxins, and damaged cell products. Accumulation of toxins, damaged cell products and unwanted proteins has been proven to play a role in aging and many forms of disease and cancer.

TRIF/TICAM1 and mitochondrial dynamics in the innate immune response

TRIF, also known as toll like receptor adaptor molecule 1 or TICAM1, is known for its role in invading foreign pathogens as part of our innate immune response. TRIF/TICAM1 is a TIR-domain adaptor protein (toll/interleukin-1 receptor) that interacts with the Toll-like receptors (TLRs) through intracellular signaling and recognition of its TIR site.

Tat-Beclin 1: The pioneering of an autophagy-inducing peptide

Autophagy is an essential process that maintains cellular homeostasis and carries out lysosome-mediated degradation of unwanted proteins in the cytoplasm.  Because of this regulatory function, autophagy is often examined when looking at disease pathways.  While our immune system initiates the removal of viruses and pathogens through the autophagic pathway, viruses, such as HIV, have developed a way to evade this process through inhibition.  Therefore, developing a reliable way to examine the molecular process of this inhibition and interaction is very desired.  The central autophagy

Three things everyone studying autophagy should know

Novus Biologicals' antibodies are the gold standard to monitor autophagy and detect LC3 expression. The recently published Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (3rd Edition) comprehensively details methods to monitor autophagy in cell or tissue samples. Importantly, these guidelines also provide key considerations for data interpretation and tips to creating better western blot data.