Autophagy Related 3 Homolog/ATG3 Protein(C-6His, N-T7 tag) (recombinant human)

Protein Construction: Recombinant Human Ubiquitin-like-conjugating Enzyme ATG3/ATG3 is produced by our E.coli expression system and the target gene encoding Met1-Met314 is expressed. Sequence: Met 1-Met314. Fusion tag: C-6His Endotoxin: < 1.0 EU per µg as determined by the LAL method. Apparent Molecular Mass: 38 kDa. Protein function: Ubiquitin-like-conjugating enzyme ATG3 (ATG3), also known as Apg3L and Apg3p, functions as a regulatory component of autophagosome biogenesis necessary for autophagy. ATG3 exhibits 98% aa sequence identity with both its mouse and rat orthologs. It is widely expressed and has highly levels in heart, skeletal muscle, kidney, liver and placenta. As an E2-like enzyme, involves in autophagy and mitochondrial homeostasis. ATG3 catalyzes the conjugation of ATG8-like proteins to PE which is essential for autophagy. ATG3 also can catalyze the conjugation of ATG12 to itself which palys a role in mitochondrial homeostasis but not in autophagy. Protein function: E2 conjugating enzyme required for the cytoplasm to vacuole transport (Cvt), autophagy, and mitochondrial homeostasis. Responsible for the E2-like covalent binding of phosphatidylethanolamine to the C-terminal Gly of ATG8-like proteins (GABARAP, GABARAPL1, GABARAPL2 or MAP1LC3A). The ATG12- ATG5 conjugate plays a role of an E3 and promotes the transfer of ATG8-like proteins from ATG3 to phosphatidylethanolamine (PE). This step is required for the membrane association of ATG8-like proteins. The formation of the ATG8-phosphatidylethanolamine conjugates is essential for autophagy and for the cytoplasm to vacuole transport (Cvt). Preferred substrate is MAP1LC3A. Also acts as an autocatalytic E2-like enzyme, catalyzing the conjugation of ATG12 to itself, ATG12 conjugation to ATG3 playing a role in mitochondrial homeostasis but not in autophagy. ATG7 (E1-like enzyme) facilitates this reaction by forming an E1-E2 complex with ATG3. Promotes primary ciliogenesis by removing OFD1 from centriolar satellites via the autophagic pathway. [The UniProt Consortium]