A major contributor to cellular homeostasis is the ability of the cell to strike a balance between the formation and degradation/removal of its cellular components. This process of internal cellular turn-over is called autophagy (self-eating), and is facilitated by a pathway of around 16 interacting proteins in the human. LC3, a ubiquitin-like modifier protein, is the human homolog of yeast Apg8 and is involved in the formation of autophagosomal vacuoles, called autophagosomes. LC3 is expressed as 3 splice variants (LC3A, LC3B and LC3C), which exhibit different tissue distributions and are processed into cytosolic and autophagosomal membrane-bound forms, termed LC3-I and LC3-II, respectively. A disruption to the autophagic process is now associated with the progression of several cancers, neurodegenerative disorders and cardiac pathologies, where LC3 is widely employed as a marker for autophagy.
Function: Probably involved in formation of autophagosomal vacuoles (autophagosomes).
Subunit: 3 different light chains, LC1, LC2 and LC3, can associate with MAP1A and MAP1B proteins. Interacts with SQSTM1. Interacts with TP53INP1 and TP53INP2.
Subcellular Location: Cytoplasmic. Endomembrane system; Lipid-anchor. Cytoplasmic vesicle, autophagosome membrane; Lipid-anchor. Note: LC3B binds to the autophagic membranes.
Tissue Specificity: Most abundant in heart, brain, liver, skeletal muscle and testis but absent in thymus and peripheral blood leukocytes.
Post-translational modifications: The precursor molecule is cleaved by APG4B/ATG4B to form the cytosolic form, LC3-I. This is activated by APG7L/ATG7, transferred to ATG3 and conjugated to phospholipid to form the membrane-bound form, LC3-II.