Apolipoprotein H / APOH Antibody

Apolipoprotein H / APOH Antibody Datasheet

Apolipoprotein H / APOH Antibody Product Information

• Immunogen: Recombinant Human APOH protein (Catalog#11221-H08H)
• Antibody Type: Rabbit Monoclonal Antibody ( Rabbit mAb Service Platform )
• Clone ID: 003
• Ig Type: Rabbit IgG
• Formulation: 0.2 μm filtered solution in PBS with 5% trehalose
• Preparation: This antibody was obtained from a rabbit immunized with purified, recombinant Human Apolipoprotein H / APOH (rh Apolipoprotein H / APOH; Catalog#11221-H08H; NP_000033.2; Met 1-Cys345).

Apolipoprotein H / APOH Antibody Usage Guide

• Specificity: Human Apolipoprotein H / APOH
• Western blot: This antibody can be used at 1-2 μg/mL with the appropriate secondary reagents to detect Human APOH in WB. Using a DAB detection system, the detection limit for Human APOH is approximately 0.25 ng/lane under non-reducing conditions.Use of this antibody under reducing conditions is not recommended.
• Direct ELISA: This antibody can be used at 0.1-0.2 μg/mL with the appropriate secondary reagents to detect Human APOH. The detection limit for Human APOH is approximately 0.00975 ng/well.
• Storage: This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -70℃. Preservative-Free.
  Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.

Apolipoprotein H / APOH Antibody Background

Beta-2-glycoprotein 1, also known as Apolipoprotein H, Activated protein C-binding protein, APOH, B2GPI, and B2G1, is a glycoprotein synthesized by liver cells and it is present in the blood associated with plasma lipoproteins. APOH binds to various kinds of negatively charged substances such as heparin, phospholipids, and dextran sulfate. APOH may prevent activation of the intrinsic blood coagulation cascade by binding to phospholipids on the surface of damaged cells. APOH appears to completely inhibitserotoninrelease by the platelets and prevents subsequent waves of the ADP-induced aggregation. The activity of APOH appears to involve the binding of agglutenating, negatively charged compounds, and inhibits agglutenation by the contact activation of the intrinsic blood coagulation pathway. APOH causes a reduction of the prothrombinase binding sites on platelets and reduces the activation caused by collagen when thrombin is present at physiological serum concentrations of APOH suggesting a regulatory role of APOH in coagulation. APOH plasma concentrations are strongly associated to metabolic syndrome alterations and vascular disease in type 2 diabetic and could be considered as a clinical marker of cardiovascular risk.

References

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