Autophagy-related protein 7 (ATG7) (ATG7)

Autophagy-related protein 7 (ATG7) is a critical E1-like activating enzyme that plays a central role in the autophagy pathway, a conserved cellular degradation process [1]. It is responsible for the activation of ATG12 and ATG8 (LC3) proteins, which are essential for the formation and expansion of the autophagosome membrane [1, 4]. In the context of disease, ATG7-mediated autophagy often acts as a survival mechanism for cancer cells under metabolic stress or during chemotherapy, making it an attractive target for sensitizing tumors to treatment [2]. Conversely, loss of ATG7 function is associated with the accumulation of damaged organelles and protein aggregates, contributing to neurodegenerative and metabolic disorders [3]. Therapeutic strategies targeting ATG7 mRNA, such as antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs), aim to downregulate ATG7 expression to inhibit autophagy in specific pathological contexts like oncology [2]. However, because autophagy is vital for maintaining cellular homeostasis in healthy tissues, therapeutic window and tissue-specific delivery remain significant challenges [3]. ATG7 also participates in non-canonical functions such as cell cycle regulation and secretion, further complicating the potential effects of its inhibition [1]. Monitoring biomarkers like LC3-II conversion and p62 accumulation is essential for assessing the efficacy of ATG7-targeted interventions [2].

Other names

APG7APG7LGSA7Autophagy-related 7-like proteinUbiquitin-activating enzyme E1-like protein ATG7

Inhibition of ATG7 protein synthesis via RNA interference (siRNA) or antisense oligonucleotide (ASO) mediated degradation of ATG7 mRNA, thereby blocking the E1-like activation of ATG12 and LC3 and preventing autophagosome formation [2].