Human Serpin A8, His Tag (SE8-H5227) is expressed from human 293 cells (HEK293). It contains AA Asp 34 - Ala 485 (Accession # NP_000020.1).
Predicted N-terminus: Asp 34
This protein carries a polyhistidine tag at the C-terminus.
The protein has a calculated MW of 50.6 kDa. The protein migrates as 55-60 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.
Less than 1.0 EU per μg by the LAL method.
>98% as determined by SDS-PAGE.
Lyophilized from 0.22 μm filtered solution in PBS, pH7.4. 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.
No activity loss is observed after storage at:
- 4-8°C for 12 months in lyophilized state;
- -70°C for 3 months under sterile conditions after reconstitution.
Human Serpin A8, 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 98%.
Serpin A8 also known as angiotensinogen (AGT) , is a member of the serpin family. It is an α-2-globulin that is expressed by the liver and secreted in plasma. As essential component of the renin-angiotensin system (RAS), Angiotensinogen is cleaved into three chains: Angiotensin-1 (Ang I), Angiotensin-2 (Ang II), and Angiotensin-3 (Ang III) in lowered blood pressure by the enzyme renin. Angiotensin-1 is a substrate of ACE (angiotensin converting enzyme) that removes a dipeptide to yield the physiologically active peptide angiotensin-2. Angiotensin-2 acts directly on vascular smooth muscle as a potent vasoconstrictor, affects cardiac contractility and heart rate through its action on the sympathetic nervous system, and alters renal sodium and water absorption through its ability to stimulate the zona glomerulosa cells of the adrenal cortex to synthesize and secrete aldosterone. Angiotensin-3 stimulates aldosterone release. Defects in AGT are a cause of renal tubular dysgenesis (RTD).
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