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Human Properdin Protein, His Tag

分子别名(Synonym)

Properdin,Complement factor P,CFP,PFC

表达区间及表达系统(Source)

Human Properdin, His Tag (PRN-H52H3) is expressed from human 293 cells (HEK293). It contains AA Asp 28 - Leu 469 (Accession # P27918-1).

Predicted N-terminus: Asp 28

蛋白结构(Molecular Characterization)

Online(Asp 28 - Leu 469) P27918-1

This protein carries a polyhistidine tag at the C-terminus.

The protein has a calculated MW of 50.7 kDa. The protein migrates as 55 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.

内毒素(Endotoxin)

Less than 1.0 EU per μg by the LAL method.

纯度(Purity)

>90% as determined by SDS-PAGE.

制剂(Formulation)

Lyophilized from 0.22 μm filtered solution in PBS, pH7.4. Normally trehalose is added as protectant before lyophilization.

Contact us for customized product form or formulation.

重构方法(Reconstitution)

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

存储(Storage)

For long term storage, the product should be stored at lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:

  1. -20°C to -70°C for 12 months in lyophilized state;
  2. -70°C for 3 months under sterile conditions after reconstitution.
 

电泳(SDS-PAGE)

Human Properdin, His Tag (Cat. No. PRN-H52H3) SDS-PAGE gel

Human Properdin, 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 90%.

背景(Background)

Properdin is also known as Complement factor P, CFP, PFC, a positive regulator of the alternate pathway of complement. It binds to and stabilizes the C3- and C5-convertase enzyme complexes. Properdin is produced by many different leukocyte subsets and circulates as cyclic oligomers of monomeric subunits. Properdin on platelet/granulocyte aggregates(PGA) formation are tightly regulated by Factor H, properdin enhances PGA formation via increased production of C5a, and that inhibition of properdin function has therapeutic potential to limit thromboinflammation in diseases characterized by increased PGA formation.

 

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