Human Complement C5, His Tag (CO5-H52Ha) is expressed from human 293 cells (HEK293). It contains AA Gln 19 - Cys 1676 (Accession # P01031-1).
Predicted N-terminus: Gln 19
This protein carries a polyhistidine tag at the C-terminus.
The protein has a calculated MW of 188.2 kDa. The protein migrates as 66 kDa and 110 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.
Less than 1.0 EU per μg by the LAL method.
>90% as determined by SDS-PAGE.
Lyophilized from 0.22 μm filtered solution in PBS, pH7.4. Normally trehalose 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.
No activity loss was observed after storage at:
- 4-8°C for 12 months in lyophilized state;
- -70°C for 3 months under sterile conditions after reconstitution.
Human Complement C5, 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%.
Derived from proteolytic degradation of complement C5, C5 anaphylatoxin is a mediator of local inflammatory process. C5 precursor is first processed by the removal of 4 basic residues, forming two chains, beta and alpha, linked by a disulfide bond. C5 convertase activates C5 by cleaving the alpha chain, releasing C5a anaphylatoxin and generating C5b (beta chain + alpha' chain). Activation of C5 by a C5 convertase initiates the spontaneous assembly of the late complement components, C5-C9, into the membrane attack complex. C5b has a transient binding site for C6. The C5b-C6 complex is the foundation upon which the lytic complex is assembled. The C5a anaphylatoxin interacts with C5AR1 and tick complement inhibitor. C5a is also a potent chemokine which stimulates the locomotion of polymorphonuclear leukocytes and directs their migration toward sites of inflammation.