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affinity biologicals/Protein C Deficient - Depleted Plasma/PC-DP
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affinity biologicals/Protein C Deficient - Depleted Plasma/PC-DP
品牌 / 
affinity
货号 / 
PC-DP
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Description

Protein C Deficient – Depleted Plasma

Protein C Deficient – Depleted Plasma is manufactured from normal citrated human plasma that has been depleted of Protein C Deficient – Depleted Plasma by selective affinity immuno-adsorption using antibodies directed towards Protein C.  Available in two different formats – Frozen and Lyophilized

Only the highest quality citrated plasma is used as starting material and in many cases the parent plasma is available as control material.  Our Protein C Deficient – Depleted Plasma can be used for further manufacturing or research use only applications.


Frozen Protein C Deficient Plasma

Product Code:  PC-DP

Presentation:  Frozen Protein C Deficient – Depleted Plasma

Preparation/Handling:  Thaw 1 ml vials in 37oC water bath for 5 minutes; for bulk volumes, thawing time will be dependent on bottle size.

Storage and Stability:  Plasma is shipped frozen and should be stored below -60oC. Product is stable until date stated on vial label when stored at -60oC. Once thawed, plasma is stable for 4 hours at 2-8oC in original vial.

Certificate of Analysis:  available upon request

Lyophilized Protein C Deficient Plasma

Product Code:  PC-LDP

Presentation:  Freeze Dried Protein C Deficient – Depleted Plasma containing 50 mM HEPES and stabilizers.

Reconstitution: Reconstitute with 1 mL of reagent grade water.  Allow contents to dissolve for 15 minutes at room temperature with occasional swirling.  Stability after reconstitution is 4 hours at ambient (18-25oC), or 30 days at –20oC.

Storage and Stability:  Prior to reconstitution, dried plasma should be stored at 2-8°C.  Product is stable until date stated on vial label when stored at 2-8oC.  Stability after reconstitution is 4 hours at ambient (18-25oC), or 30 days at –20oC.

Certificate of Analysis:  available upon request

Description of Protein C

Protein C is a vitamin K-dependent glycoprotein produced in the liver. The concentration of PC in plasma is ~4 μg/ml (~60 nM). A deficiency of Protein C (quantitative or qualitative) is a risk factor for vascular thrombosis. Protein C is expressed as a two-chain molecule with a molecular weight of 62 kDa. The light chain (21 kDa) of PC consists of two EGF-like domains and an amino-terminal domain containing one hydroxyaspartic acid and 11 γ-carboxyglutamic acid (gla) residues. These residues allow PC to bind to membranes that contain acidic phospholipids in a calcium dependent manner. The heavy chain of PC (41 kDa) consists of the catalytic domain and an activation peptide. Activation of Protein C results from cleavage at residue Arg12 in the heavy chain by a complex of thrombin and a cell surface cofactor thrombomodulin. The activation of PC is associated with the release of a small activation peptide (2-3 kDa, called Protein C peptide, or PCP) from the N-terminal of the heavy chain. Activated Protein C (APC) is a serine protease with anticoagulant activity. APC, in complex with a phospholipid membrane, calcium and the Protein S cofactor, exhibits anticoagulant activity through the proteolytic inactivation of coagulation cofactors Va and VIIIa. The primary inhibitor of APC activity in plasma is Protein C Inhibitor (PCI, also called Plasminogen Activator Inhibitor-3, PAI-3) and to a lesser extent by α1antitrypsin and α2macroglobulin. The inhibitory activity of PCI is stimulated approximately 10 fold by heparin1-3.

References and Reviews

  1. Broze GJ, Miletich JP; Biochemistry and Physiology of Protein C, Protein S and Thrombomodulin; in Hemostasis and Thrombosis, 3rd Edition, eds. RW Colman, J Hirsh, VJ Marder and EW Salzman, pp 259-276, J.B. Lippincott Co., Philadelphia PA, USA, 1994.
  2. Esmon CT, Esmon NL, Le Bonniec B, Johnson AE; Protein C Activation; Methods in Enzymology 222, pp 359-385, 1993.
  3. Heeb MJ, Mosher D, Griffin JH; Activation and Complexation of Protein C and Cleavage and Decrease of Protein S in Plasma of Patients With Intravascular Coagulation; Blood 73, pp 455-461, 1989.

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