CFD,Adipsin,PFD,DF,Complement factor D
Human Complement Factor D, His Tag (CFD-H52H8) is expressed from human 293 cells (HEK293) and active. It contains AA Ile 26 - Ala 253 (Accession # P00746-1).
Predicted N-terminus: Ile 26
This protein carries a polyhistidine tag at the C-terminus.
The protein has a calculated MW of 26.3 kDa. The protein migrates as 28 kDa under non-reducing (NR) condition (SDS-PAGE) due to glycosylation.
Less than 1.0 EU per μg by the LAL method.
>95% as determined by SDS-PAGE.
Lyophilized from 0.22 μm filtered solution in 50 mM Tris, 150 mM NaCl, pH8.0. Normally glycerol is added as protectant before lyophilization.
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Please see Certificate of Analysis for specific instructions.
For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.
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:
- -20°C to -70°C for 12 months in lyophilized state;
- -70°C for 3 months under sterile conditions after reconstitution.
Human Complement Factor D, His Tag on SDS-PAGE under non-reducing (NR) condition. The gel was stained overnight with Coomassie Blue. The purity of the protein is greater than 95%.
Measured by its ability to cleave a colorimetric peptide substrate, N-carbobenzyloxy-Lys-ThioBenzyl ester (Z-Lys-SBzl), in the presence of 5,5’Dithio-bis (2-nitrobenzoic acid) (DTNB). The specific activity is >80 pmol/min/μg (QC tested).
Complement factor D (CFD) is also known as Adipsin, C3 convertase activator, Properdin factor D (PFD), which contains one peptidase S1 domain and belongs to the peptidase S1 family. CFD / Adipsin cleaves factor B when the latter is complexed with factor C3b, activating the C3bbb complex, which then becomes the C3 convertase of the alternate pathway. CFD / Adipsin is a serine protease that stimulates glucose transport for triglyceride accumulation in fats cells and inhibits lipolysis. Defects in CFD / Adipsin are the cause of complement factor D deficiency which predisposes to invasive meningococcal disease.