Anti-APG5L/ATG5 Antibody Picoband®, PE Conjugate

Autophagy protein 5 is a protein that in humans is encoded by the ATG5 gene. It is also known as APG5 or ASP, and this gene is mapped to 6q21. It is found that knockdown of ATG5 in hepatocytes increased triglyceride levels with oleate or a second endogenous stimulus for triglyceride formation. These hepatocytes with ATG5 knockdown also had increased lipid droplet number and size. ATG5 is an E3 ubiquitin ligase which is necessary for autophagy due to its role in autophagosome elongation. It is activated by ATG7 and forms a complex with ATG12 and ATG16L1. This complex is necessary for LC3-1 conjugation to PE to form LC3-II.

A synthetic peptide corresponding to a sequence in the middle region of human APG5L, identical to the related mouse sequence, and different from the related rat sequence by one amino acid.

Ubiquitous. The mRNA is present at similar levels in viable and apoptotic cells, whereas the protein is dramatically highly expressed in apoptotic cells.

Involved in autophagic vesicle formation. Conjugation with ATG12, through a ubiquitin-like conjugating system involving ATG7 as an E1-like activating enzyme and ATG10 as an E2-like conjugating enzyme, is essential for its function. The ATG12-ATG5 conjugate acts as an E3-like enzyme which is required for lipidation of ATG8 family proteins and their association to the vesicle membranes. Involved in mitochondrial quality control after oxidative damage, and in subsequent cellular longevity. The ATG12- ATG5 conjugate also negatively regulates the innate antiviral immune response by blocking the type I IFN production pathway through association with RARRES3 and MAVS. Also plays a role in translation or delivery of incoming viral RNA to the translation apparatus. Plays a critical role in multiple aspects of lymphocyte development and is essential for both B and T lymphocyte survival and proliferation. Required for optimal processing and presentation of antigens for MHC II. Involved in the maintenance of axon morphology and membrane structures, as well as in normal adipocyte differentiation. Promotes primary ciliogenesis through removal of OFD1 from centriolar satellites and degradation of IFT20 via the autophagic pathway.

1. Baumann P, Cech TR (May 2001). "Pot1, the putative telomere end-binding protein in fission yeast and humans". Science 292 (5519): 1171–5. 2. Hammond EM, Brunet CL, Johnson GD, Parkhill J, Milner AE, Brady G, Gregory CD, Grand RJ (May 1998). "Homology between a human apoptosis specific protein and the product of APG5, a gene involved in autophagy in yeast". FEBS Lett 20 (3): 391–5. 3. Singh, R., Kaushik, S., Wang, Y., Xiang, Y., Novak, I., Komatsu, M., Tanaka, K., Cuervo, A. M., Czaja, M. J. Autophagy regulates lipid metabolism. Nature 458: 1131-1135, 2009.

Store at -20℃ for one year from date of receipt. After reconstitution, at 4℃ for one month. It can also be aliquotted and stored frozen at -20℃ for six months. Avoid repeated freeze-thaw cycles.

Cytoplasm. Preautophagosomal structure membrane; Peripheral membrane protein. Colocalizes with nonmuscle actin. The conjugate detaches from the membrane immediately before or after autophagosome formation is completed (By similarity). Localizes also to discrete punctae along the ciliary axoneme and to the base of the ciliary axoneme. .