Immunofluorescent analysis of ATG9A showing staining in the cytoplasm of U-251 cells. U251 cells were treated with Chloroquine (50uM,16h), fixed with 4% PFA (20 min) and permeabilized with Triton X-100 (0.2%, 30 min). Cells were probed with an ATG9A polyclonal antibody (Product # PA5-35205) (1:100, 2h at room temperature) followed by detection using a fluorescent conjugated secondary antibody (green) (1:1000, 1h). Nuclei were stained with Hoechst 33342 (blue) (10 ug/ml, 5 min).
|Tested species reactivity||Human|
|Host / Isotype||Rabbit / IgG|
|Immunogen||KLH conjugated synthetic peptide between 717-746 amino acids from the C-terminal region of human ATG9A|
|Purification||Antigen affinity chromatography|
|Contains||0.09% sodium azide|
|Storage Conditions||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C|
|Tested Applications||Dilution *|
|Immunohistochemistry (Paraffin) (IHC (P))||1:50-1:100|
|Western Blot (WB)||1:1000|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
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.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.