Rabbit Recombinant Monoclonal ATG9A antibody - conjugated to Alexa Fluor® 594.
pH: 7.4
Preservative: 0.02% Sodium azide
Constituents: 68% PBS, 30% Glycerol (glycerin, glycerine), 1% BSA
Application | Reactivity | Dilution info | Notes |
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Application Target Binding Affinity | Reactivity Expected | Dilution info - | Notes - |
Application Antibody Labelling | Reactivity Expected | Dilution info - | Notes - |
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Phospholipid scramblase involved in autophagy by mediating autophagosomal membrane expansion (PubMed:22456507, PubMed:27510922, PubMed:29437695, PubMed:32513819, PubMed:32610138, PubMed:33106659, PubMed:33468622, PubMed:33850023). Cycles between the preautophagosomal structure/phagophore assembly site (PAS) and the cytoplasmic vesicle pool and supplies membrane for the growing autophagosome (PubMed:16940348, PubMed:22456507, PubMed:33106659). Lipid scramblase activity plays a key role in preautophagosomal structure/phagophore assembly by distributing the phospholipids that arrive through ATG2 (ATG2A or ATG2B) from the cytoplasmic to the luminal leaflet of the bilayer, thereby driving autophagosomal membrane expansion (PubMed:33106659). Also required to supply phosphatidylinositol 4-phosphate to the autophagosome initiation site by recruiting the phosphatidylinositol 4-kinase beta (PI4KB) in a process dependent on ARFIP2, but not ARFIP1 (PubMed:30917996). In addition to autophagy, also plays a role in necrotic cell death (By similarity).
APG9L1, ATG9A, Autophagy-related protein 9A, APG9-like 1, mATG9
Rabbit Recombinant Monoclonal ATG9A antibody - conjugated to Alexa Fluor® 594.
pH: 7.4
Preservative: 0.02% Sodium azide
Constituents: 68% PBS, 30% Glycerol (glycerin, glycerine), 1% BSA
The mouse and rat recommendation is based on the WB results. We do not guarantee IHC-P for mouse and rat.
This product is a recombinant monoclonal antibody, which offers several advantages including:
For more information, read more on recombinant antibodies.
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.
This conjugated primary antibody is released using a quantitative quality control method that evaluates binding affinity post-conjugation and efficiency of antibody labeling.
For suitable applications and species reactivity, please refer to the unconjugated version of this clone. This conjugated antibody is eligible for the Abcam trial program.
ATG9A also known as APG9-like 1 or ATG9 autophagy related 9A is an important component in the autophagy machinery. This protein has a molecular weight of approximately 93 kDa. It is ubiquitously expressed in various tissues with higher expression seen in the heart and skeletal muscle. Mechanically ATG9A is essential for the trafficking of membranes necessary for autophagosome formation. It actively participates in membrane lipids' delivery from donor organelles which are critical for constructing autophagosomes.
ATG9A facilitates the recycling of cellular materials through a process called autophagy. This protein acts with other autophagy-related proteins to form a complex essential for autophagosome elongation and closure. The ATG9A protein's dynamic movements between the Golgi apparatus and endosomes ensure proper membrane supply for autophagy. It coordinates with the ULK1 complex and various phospholipid-modifying enzymes which are necessary to regulate autophagic flux.
ATG9A plays an integral role in the mTOR signaling and MAPK pathways. Both pathways are essential for cellular responses to stress and nutrient availability. In these pathways ATG9A works closely with proteins like beclin 1 and ATG5. Inhibiting mTOR actively induces autophagy where ATG9A contributes to membrane recruitment and elongation of the autophagosomes facilitating the clearance of damaged organelles and proteins.
ATG9A shows a significant link to neurodegenerative diseases such as Parkinson's and Alzheimer's disease. The dysfunction of autophagic pathways due to altered ATG9A function leads to the accumulation of damaged proteins and organelles. This event contributes to the pathogenesis of such neurodegenerative diseases. Moreover ATG9A closely associates with proteins like LAMP2 whose mutations similarly lead to defective autophagic processes resulting in the accumulation of unprocessed cellular debris in these disorders.
We have tested this species and application combination and it works. It is covered by our product promise.
We have not tested this specific species and application combination in-house, but expect it will work. It is covered by our product promise.
This species and application combination has not been tested, but we predict it will work based on strong homology. However, this combination is not covered by our product promise.
We do not recommend this combination. It is not covered by our product promise.
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