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anti-Complement C3, mAb (10A1)
Product Details | |
---|---|
Synonyms | C3; CPAMD1 |
Product Type | Monoclonal Antibody |
Properties | |
Clone | 10A1 |
Isotype | Mouse IgG2b κ |
Immunogen/Antigen | Complement C3 protein purified from human plasma. |
Application |
ELISA |
Crossreactivity | Human |
Purity Detail | Ammonium sulfate precipitation. |
Formulation | Liquid. HEPES with 0.15M NaCl, 0.01% BSA, 0.03% sodium azide, and 50% glycerol. |
Isotype Negative Control | |
Other Product Data |
Click here for Original Manufacturer Product Datasheet |
Declaration | Manufactured by AbFrontier |
Shipping and Handling | |
Shipping | BLUE ICE |
Short Term Storage | +4°C |
Long Term Storage | -20°C |
Use/Stability | Stable for at least 1 year after receipt when stored at -20°C. |
Documents | |
MSDS | Inquire |
Product Specification Sheet | |
Datasheet |
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Human Complement C3 (C3) is synthesized as a single-chain pro-molecule (185 kDa) that then suffers several post-translational modifications. Before being secreted as a mature protein, C3 is split into β-chain (645 residues and 70 kDa) and α-chain (992 residues and 115 kDa) and forms a rare internal thioester bond. C3 plays a central role in the activation of all the three pathways of complement activation i.e. the classical, alternative, and lectin pathway. As C3 is the major complement component and participates in several stages of the immune response, its deficiency generally associated with higher susceptibility to severe bacterial infections and in some cases with autoimmune diseases such as systemic lupus erythematosus. C3 plays a central role in the activation of the complement system. Its processing by C3 convertase is the central reaction in both classical and alternative complement pathways. After activation C3b can bind covalently, via its reactive thioester, to cell surface carbohydrates or immune aggregates. Derived from proteolytic degradation of complement C3, C3a anaphylatoxin is a mediator of local inflammatory process. It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes.
1) Sahu, A and Lambris, J. D. (2001) Immunol Rev. 180: 35-48. (General)
2) Mueller-Eberhard, H. J.(1988) Annu. Rev. Biochem. 57: 321-47. (General)