
Gamma-aminobutyric acid (GABA) is the main inhibitory transmitter by increasing a Cl-conductance that inhibits neuronal firing in the central nervous system (1). It has been shown to activate both ionotropic (GABAA) and metabotropic (GABAB) receptors as well as a third class of receptors called GABAC (2). GABARAPL2 (GABAA receptor-associated protein-like 2), also known as GATE16, was initially identified as a membrane transport modulator and is a mammalian ortholog to the autophagy protein ATG8 (3,4). It is thought that GABARAPL2 and other members of the ATG8 family act as scaffolds for assembly of the Unc-51 like kinase (ULK) complex in the formation of autophagosomes (5).
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