Mouse ADAM17, His Tag (AD7-M52H1) is expressed from human 293 cells (HEK293). It contains AA Pro 18 - Asp 563 (Accession # Q9Z0F8).
Predicted N-terminus: Pro 18, Asp 59 and Arg 215
This protein carries a polyhistidine tag at the C-terminus.
The protein has a calculated MW of 63.4 kDa. The protein migrates as 19 kDa and 20 kDa (Propeptide), 55-66 kDa (Mature-ADAM17) and 75-94 kDa (Pro-ADAM17) under reducing (R) condition (SDS-PAGE) due to glycosylation.
Less than 1.0 EU per μg by the LAL method.
>85% as determined by SDS-PAGE.
Lyophilized from 0.22 μm filtered solution in 50 mM MES, 150 mM NaCl, pH6.5. Normally trehalose is added as protectant before lyophilization.
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Please see Certificate of Analysis for specific instructions.
For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.
For long term storage, the product should be stored at lyophilized state at -20°C or lower.
Please avoid repeated freeze-thaw cycles.
This product is stable after storage at:
- -20°C to -70°C for 12 months in lyophilized state;
- -70°C for 3 months under sterile conditions after reconstitution.
Mouse ADAM17, His Tag on SDS-PAGE under reducing (R) condition. The gel was stained overnight with Coomassie Blue. The purity of the protein is greater than 85%.
Disintegrin and metalloproteinase domain-containing protein 17 (ADAM17), a member of the ADAM protein family of disintegrins and metalloproteases, is also known as TNF-alpha convertase, TNF-alpha-converting enzyme and CD156b, which contains one disintegrin domain and one peptidase M12B domain. ADAM17 can cleave the membrane-bound precursor of TNF-alpha to its mature soluble form. ADAM17 is also responsible for the proteolytical release of soluble JAM3 from endothelial cells surface (By similarity) and proteolytic release of several other cell-surface proteins, including p75 TNF-receptor, interleukin 1 receptor type II, p55 TNF-receptor, transforming growth factor-alpha, L-selectin, growth hormone receptor, MUC1 and the amyloid precursor protein. Furthermore, ADAM17 acts as an activator of Notch pathway by mediating cleavage of Notch, generating the membrane-associated intermediate fragment called Notch extracellular truncation.