|Application ||WB, IHC-P, FC, E|
|Calculated MW||122205 Da|
|Antigen Region||547-577 aa|
|Other Names||Ceruloplasmin, Ferroxidase, CP|
|Target/Specificity||This CP antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 547-577 amino acids from the Central region of human CP.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||CP Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Ceruloplasmin is a blue, copper-binding (6-7 atoms per molecule) glycoprotein. It has ferroxidase activity oxidizing Fe(2+) to Fe(3+) without releasing radical oxygen species. It is involved in iron transport across the cell membrane. Provides Cu(2+) ions for the ascorbate-mediated deaminase degradation of the heparan sulfate chains of GPC1. May also play a role in fetal lung development or pulmonary antioxidant defense (By similarity).|
|Cellular Location||Secreted. Note=Colocalizes with GCP1 in secretory intracellular compartments.|
|Tissue Location||Expressed by the liver and secreted in plasma.|
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abgent to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
CP is a metalloprotein that binds most of the copper in plasma and is involved in the peroxidation of Fe(II)transferrin to Fe(III) transferrin. Mutations in this protein cause aceruloplasminemia, which results in iron accumulation and tissue damage, and is associated with diabetes and neurologic abnormalities.
Park,Y., Lee,I.S. Arch. Pharm. Res. 32 (5), 693-698 (2009)
Altamura,C., Squitti,R. Stroke 40 (4), 1282-1288 (2009)
Squitti,R., Quattrocchi,C.C. Prion 2 (1), 23-27 (2008)
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