Recombinant Mouse Ceruloplasmin/CP protein (His tag)
SKU: PDEM100040-100
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Recombinant Mouse Ceruloplasmin/CP protein (His tag)
SKU # | PDEM100040 |
Expression Host | E. coli |
Description
Synonyms | CERU_MOUSE;EC:1.16.3.1;Ferroxidase |
Species | Mouse |
Expression_host | E.coli |
Sequence | Tyr729-Gly1061 |
Accession | Q61147 |
Mol_Mass | 36.5 kDa |
AP_Mol_Mass | 40 kDa |
Tag | N-His |
Bio_Activity | Not validated for activity |
Properties
Purity | > 95 % as determined by reducing SDS-PAGE. |
Endotoxin level | Please contact us for more information. |
Storage | Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months. |
Shipping | This product is provided as lyophilized powder which is shipped with ice packs. |
Formulation | Lyophilized from sterile PBS, pH 7.4. Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization. Please refer to the specific buffer information in the printed manual. |
Reconstitution | It is recommended that sterile water be added to the vial to prepare a stock solution of 0.5 mg/mL. Concentration is measured by UV-Vis |
Background
Ceruloplasmin is a blue, copper-binding (6-7 atoms per molecule) glycoprotein. It has ferroxidase activity oxidizing Fe2+ to Fe3+ without releasing radical oxygen species. It is involved in iron transport across the cell membrane. Provides Cu2+ 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. Defects in CP are the cause of aceruloplasminemia (ACERULOP) [MIM:604290]. It is an autosomal recessive disorder of iron metabolism characterized by iron accumulation in the brain as well as visceral organs. Clinical features consist of the triad of retinal degeneration, diabetes mellitus and neurological disturbances. Note=Ceruloplasmin levels are decreased in Wilson disease, in which copper cannot be incorporated into ceruloplasmin in liver because of defects in the copper-transporting ATPase 2.