ATG10 is central to autophagy through two ubiquitin-like conjugation systems:
ATG12-ATG5 Conjugation:
Isoform-Specific Roles:
ATG10 (Long Isoform): Promotes autophagosome formation but traps vesicles peripherally, impairing lysosomal fusion and autophagy flux. Enhances HCV replication .
ATG10S (Short Isoform): Lacks 36 N-terminal residues, drives autophagosomes to lysosome-rich perinuclear regions, facilitating HCV RNA degradation .
Isoform | Length | Function | Impact on HCV |
---|---|---|---|
ATG10 | 220 aa | Supports autophagosome formation | Increases replication |
ATG10S | 184 aa | Enhances autophagolysosome formation | Suppresses replication |
HCV Subgenomic Replicon:
Acute Myeloid Leukemia (AML):
Autophagy Related 10 (ATG10) is a protein coding gene that plays a crucial role in the autophagy process, which is a cellular degradation mechanism essential for maintaining cellular homeostasis. Autophagy involves the degradation of cytosolic components through lysosomes, and ATG10 is integral to this process .
The human recombinant ATG10 protein is typically produced in Escherichia coli (E. coli) expression systems. The recombinant protein consists of a single polypeptide chain containing 243 amino acids, with a molecular mass of approximately 27.7 kDa. It is often fused to a 23 amino acid His-tag at the N-terminus to facilitate purification through chromatographic techniques .
The primary function of ATG10 is to facilitate the autophagy process by acting as an E2-like enzyme. It is involved in the conjugation of ATG12 to ATG5, which is necessary for the formation of autophagosomes. These autophagosomes play a vital role in degrading and recycling cellular components, thus maintaining cellular homeostasis .
The activity of ATG10 is regulated through various cellular signals that control the autophagy process. These signals can be influenced by factors such as nutrient availability, cellular stress, and other environmental conditions. Proper regulation of ATG10 is essential for maintaining the balance between cellular degradation and synthesis .