p62

By Jamshed Arslan, Pharm. D., PhD.

By Jamshed Arslan, Pharm. D., PhD.

By Christina Towers, PhD.

By Yoskaly Lazo-Fernandez, PhD

By Jamshed Arslan Pharm.D.

By Yoskaly Lazo-Fernandez, PhD

By Christina Towers, PhD

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.

Autophagy is a crucial intracellular pathway that manages the degradation and recycling of long-lived proteins in the cell. The LC3 (or light chain 3) family is composed of three members, LC3A, LC3B and LC3C. Upon autophagy induction, LC3 is cleaved, causing the release of a C-terminal glycine that is required for phospholipid conjugation.  This process is vital to the formation of the autophagosome, a double membrane structure that delivers proteins to the lysosome during autophagy.

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