Autophagy independent roles of the core ATG proteins

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

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

Autophagy’s Paradoxical Role in ALS

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.

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

ATG4B - a cysteine protease involved in autophagosome elongation

Autophagy can be broken down into 4 main stages: phagophore nucleation, autophagosome elongation, autophagosome docking and fusion with a lysosome, and vesicle breakdown and degradation. ATG4B is one of four ATG4 homologs (ATG4A, ATG4B, ATG4C, and ATG4D) involved in autophagosome elongation. ATG4B encodes a 48 kDa protein called autophagin-1 that is a member of the C54 family of cysteine proteases.

ATG7 - an E1 enzyme for the ubiquitin-like autophagy proteins

Autophagy is an essential cellular process that maintains homeostasis through the degradation and recycling of cytoplasmic organelles and macromolecules. Substrates targeted for autophagy are engulfed in a double-membrane structure called the autophagosome which is then targeted to the lysosome for degradation. The initiation of autophagy requires two separate ubiquitin-like protein (UBL) systems that regulate autophagosome assembly. In these systems Atg7 acts as an E1-like enzyme for the UBLs Atg12 and Atg8.

ATG12 - a ubiquitin-like protein essential for autophagosome assembly

Atg12 is a ubiquitin-like protein that plays an essential role in cellular homeostasis by regulating the degradation and recycling of cytoplasmic organelles and macromolecules. Atg12 is one of two ubiquitin-like protein systems that is required during the early steps of autophagosome formation. Upon the initiation of phagopore assembly Atg12 is activated by binding to the E1-like enzyme Atg7 and is then transferred to the E2 enzyme Atg10.

Essential to Death: ATG5 (autophagy protein 5, apoptosis-specific protein ASP)

The ATG5 protein belongs to the ATG autophagy regulator family. This family controls the highly conserved cell's homeostatic response to a wide variety of both self- and foreign-originating cellular stimuli. ATG5 itself is ubiquitously expressed in most cells and most often found co-localized with the cytoplasmic non-muscle actin protein under normal resting conditions. Upon activation of apoptosis, ATG5 expression is then dramatically intensified, with ATG5 directly complexing with its ATG family members to produce autophagosomes.