Product Name: ATR Antibody
Species Reactivity: Human, Mouse, Rat
Tested Applications: ELISA, IF, IHC-P, WB
Applications: ATR antibody can be used for detection of ATR by Western blot at 0.5 to 2 μg/mL. Antibody can also be used for immunohistochemistry starting at 2 μg/mL. For immunofluorescence start at 10 μg/mL.
User Note: Optimal dilutions for each application to be determined by the researcher.
Predicted Molecular Weight: Predicted: 36, 40, 60 kDa Observed: 45 kDa
Immunogen: ATR antibody was raised against a peptide corresponding to 13 amino acids near the center of human ATR.The immunogen is located within amino acids 220 – 270 of ATR.
Host Species: Rabbit
Purification: ATR Antibody is Ion exchange chromatography purified.
Physical State: Liquid
CAS NO.: 1802088-50-1
Product: NCT-501
Buffer: ATR Antibody is supplied in PBS containing 0.02% sodium azide.
Concentration: 1 mg/mL
Storage Conditions: ATR antibody can be stored at 4˚C for three months and -20˚C, 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.
Clonality: Polyclonal
Conjugate: Unconjugated
Alternate Names: ATR Antibody: ATR, GAPO, TEM8, ATR, Anthrax toxin receptor 1, Tumor endothelial marker 8
Accession NO.: NP_444262
Protein Ino: 16933551
Official Symbol: ANTXR1
Geneid: 84168
Background: ATR Antibody: The Anthrax toxin receptor (ATR) was initially discovered as the tumor endothelial marker 8 (TEM8). This protein, which exists in three isoforms (36, 40, and 60 kDa), is highly expressed in tumor vessels as well as in the vasculature of developing embryos, suggesting that it may normally play a role in angiogenesis. However, it also acts as the receptor for anthrax toxin. Following the binding of this protein by the protective antigen (PA) of anthrax, PA is cleaved and heptamerizes to form the binding site for both edema factor (EF) and lethal factor (LF). This complex is then endocytosed by the cell; acidification in endosomes allows the release of EF and LF into the cytoplasm where they interfere with MAPK signaling and induce apoptosis.
PubMed ID:http://aac.asm.org/content/53/8/3462.abstract