|Other Names||Autophagy-related protein 9A, APG9-like 1, mATG9, ATG9A, APG9L1|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP1814f was selected from the S828 region of human APG9L1. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Involved in autophagy and cytoplasm to vacuole transport (Cvt) vesicle formation. Plays a key role in the organization of the preautophagosomal structure/phagophore assembly site (PAS), the nucleating site for formation of the sequestering vesicle. Cycles between a juxta-nuclear trans-Golgi network compartment and late endosomes. Nutrient starvation induces accumulation on autophagosomes. Starvation-dependent trafficking requires ULK1, ATG13 and SUPT20H.|
|Cellular Location||Cytoplasmic vesicle, autophagosome membrane; Multi-pass membrane protein. Golgi apparatus, trans-Golgi network membrane; Multi-pass membrane protein. Late endosome membrane; Multi-pass membrane protein. Endoplasmic reticulum membrane; Multi-pass membrane protein. Note=Under amino acid starvation or rapamycin treatment, redistributes from a juxtanuclear clustered pool to a dispersed peripheral cytosolic pool. The starvation- induced redistribution depends on ULK1, ATG13, as well as SH3GLB1|
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Provided below are standard protocols that you may find useful for product applications.
Macroautophagy is the major inducible pathway for the general turnover of cytoplasmic constituents in eukaryotic cells, it is also responsible for the degradation of active cytoplasmic enzymes and organelles during nutrient starvation. Macroautophagy involves the formation of double-membrane bound autophagosomes which enclose the cytoplasmic constituent targeted for degradation in a membrane bound structure, which then fuse with the lysosome (or vacuole) releasing a single-membrane bound autophagic bodies which are then degraded within the lysosome (or vacuole). Apg9 plays a direct role in the formation of the cytoplasm to vacuole targeting and autophagic vesicles, possibly serving as a marker for a specialized compartment essential for these vesicle-mediated alternative targeting pathways.
Baehrecke EH. Nat Rev Mol Cell Biol. 6(6):505-10. (2005) Lum JJ, et al. Nat Rev Mol Cell Biol. 6(6):439-48. (2005) Greenberg JT. Dev Cell. 8(6):799-801. (2005) Levine B. Cell. 120(2):159-62. (2005) Shintani T and Klionsky DJ. Science. 306(5698):990-5. (2004)
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