|Application ||WB, IHC-P, IF, E|
|Other Accession||NP_076990, 116089287|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||94447 Da|
|Application Notes||ATG9A antibody can be used for detection of ATG9A by Western blot at 1 µg/mL. Antibody can also be used for immunohistochemistry starting at 5 µg/mL. For immunofluorescence start at 20 µg/mL.|
|Reconstitution & Storage||ATG9A antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.|
|Precautions||ATG9A Antibody is for research use only and 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.
ATG9A Antibody: Autophagy, the process of bulk degradation of cellular proteins through an autophagosomic-lysosomal pathway is important for normal growth control and may be defective in tumor cells. It is involved in the preservation of cellular nutrients under starvation conditions as well as the normal turnover of cytosolic components. This process is negatively regulated by TOR (Target of rapamycin) through phosphorylation of autophagy protein APG1. ATG9A, a multi-spanning membrane protein localizing to the Golgi apparatus and late endosomes, has been proposed to mediate membrane transport to generate autophagosomes. ATG9A has also been implicated as a regulator of STING (stimulator of interferon genes)-mediated innate immune response.
Gozuacik D and Kimchi A. Autophagy as a cell death and tumor suppressor mechanism. Oncogene2004; 23:2891-906.
Kisen GO, Tessitore L, Costelli P, et al. Reduced autophagic activity in primary rat hepatocellular carcinoma and ascites hepatoma cells. Carcinogenesis1993; 14:2501-5.
Kamada Y, Funakoshi T, Shintani T, et al. Tor-mediated induction of autophagy via Apg1 protein kinase complex. J. Cell. Biol.2000; 150:1507-13.
Webber JL, Young AR, and Tooze SA. Atg9 trafficking in mammalian cells. Autophagy2007; 3:54-6.
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