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|Tested species reactivity||Human|
|Host / Isotype||Rabbit / IgG|
|Immunogen||A synthetic phosphopeptide derived from human ATR around the phosphorylation site of Ser428 (G-I-SP-P-K)|
|Purification||Antigen affinity chromatography|
|Storage buffer||Dulbecco's PBS, pH 7.4, with 150mM NaCl, 50% glycerol|
|Contains||0.02% sodium azide|
|Tested Applications||Dilution *|
|Immunohistochemistry (Paraffin) (IHC (P))||1:50-1:100|
* 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.
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.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
2310008J16Rik; 2810405N18Rik; Ataxia telangiectasia and Rad3-related protein; ATR; FRAP-related protein 1; FRAP-related protein-1; MEC1, mitosis entry checkpoint 1, homolog; Serine/threonine-protein kinase ATR; TEM8; tumor endothelial marker 8
ATR; FCTCS; FRP1; MEC1; SCKL; SCKL1