Anti-GABARAPL2 Antibody

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) .

GABARAPL2 antibody was raised against a 15 amino acid peptide near the carboxy terminus of human GABARAPL2. The immunogen is located within the last 50 amino acids of GABARAPL2.

Ubiquitous. Expressed at high levels in the brain, heart, prostate, ovary, spleen and skeletal muscle. Expressed at very low levels in lung, thymus and small intestine.

Ubiquitin-like modifier involved in intra-Golgi traffic. Modulates intra-Golgi transport through coupling between NSF activity and SNAREs activation. It first stimulates the ATPase activity of NSF which in turn stimulates the association with GOSR1 (By similarity) . Involved in autophagy. Plays a role in mitophagy which contributes to regulate mitochondrial quantity and quality by eliminating the mitochondria to a basal level to fulfill cellular energy requirements and preventing excess ROS production. Whereas LC3s are involved in elongation of the phagophore membrane, the GABARAP/GATE-16 subfamily is essential for a later stage in autophagosome maturation.