{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n MAP1LC3A (also known as LC3A) is a key autophagic effector that participates in the canonical autophagy pathway by driving the formation of autophagosomal membranes, mediating cargo recognition, and facilitating autophagosome–lysosome fusion. Upon autophagy induction, MAP1LC3A undergoes specific post‐translational modifications – including a C‐terminal proteolytic cleavage that primes it for lipidation – which promote its recruitment to autophagic membranes and enable it to serve as a scaffold for autophagy receptors. For example, its direct interaction via LC3‐interacting regions (LIRs) with proteins such as the polyubiquitin‐binding receptor p62/SQSTM1 ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "] and mitochondrial adaptors like FKBP8 ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": "] underlies the selective sequestration and degradation of protein aggregates and damaged organelles (e.g., during mitophagy)."}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In canonical autophagy, MAP1LC3A conversion to its lipidated form is central to cargo capture and the maturation of autophagosomes, whereas alternative, Atg5/Atg7‐independent pathways do not rely on this conversion ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": "]. Moreover, MAP1LC3A participates in specialized processes such as LC3‐associated phagocytosis—an autophagy‐related pathway that promotes efficient degradation of internalized dead cells and limits proinflammatory responses ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": "]. Its differential regulation is further highlighted by studies showing that the three human LC3 isoforms, including MAP1LC3A, exhibit distinct expression patterns and post‐translational processing that may confer specialized functions ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": "].\n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Beyond its canonical roles, MAP1LC3A can be co‐opted in non‐traditional contexts. In viral infections such as those caused by coronaviruses, nonlipidated forms of LC3 (including MAP1LC3A) mark double‐membrane vesicles that are hijacked to support viral replication ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": "], while during STING‐mediated immune signaling, interactions between STING and LC3 via classic LIR motifs initiate non‐canonical autophagy events ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": "]. In addition, the regulation of mitophagy through effectors such as TBC1D15 involves engagement of LC3/GABARAP proteins—including MAP1LC3A—to ensure proper encapsulation of damaged mitochondria ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": "].\n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, these findings underscore the pivotal role of MAP1LC3A in canonical autophagy, selective autophagy processes (including mitophagy and LC3‐associated phagocytosis), and even in specialized scenarios exploited by pathogens or immune signaling. Its regulated post‐translational modification and specific interactions with various autophagy receptors enable MAP1LC3A to orchestrate the diverse facets of autophagy that are critical for maintaining cellular homeostasis.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Serhiy Pankiv, Terje Høyvarde Clausen, Trond Lamark, et al. 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