Component | Usage | Quantity | Catalog # |
Anti-Rabbit C3a Polyclonal Antibody | Capture Antibody | 100 µg X 2 | KP1218U-100 |
Biotinylated Anti-Rabbit C3a Polyclonal Antibody | Detection Antibody | 50 µg | KPB1219U-050 |
Rabbit C3a Recombinant Protein | Standard | 5 µg | RP1131U-005 |
The Rabbit C3a (Complement Component 3a) Do-It-Yourself ELISA contains capture antibody, protein standard, and detection antibody for development of a Rabbit C3a ELISA. The antibodies have been determined to function in an ELISA with the standard provided. Optimal buffers, concentrations, incubation times, incubation temperatures, and methods for the ELISA have not been determined. A working knowledge of ELISA is strongly recommended. The quantities of components provided are not matched. Components may also be purchased separately.
For additional tips and techniques to ensure a successful ELISA, check out our ELISA Technical Guide.
C3a is an effector molecule of both the classical and alternative complement pathways for a broad range of functions including T cell activation and survival, angiogenesis stimulation, chemotaxis, mast cell degranulation, and macrophage activation. C3a produces both pro- and anti-inflammatory responses. C3a, a 77 amino acid long anaphylatoxin, is produced when C3 convertases act on the N-terminal chain of the C3 protein. The activation of the C3 protein fragments it into two proteins. The smaller protein, C3a, promotes an inflammatory reaction while the larger, called C3b, binds to the surface of many microbial cells. The binding of C3a to the specific G protein-coupled receptor, C3aR, has been shown to be involved in several diseases such as rheumatoid arthritis, septic shock syndrome, age-related macular degeneration, and asthma. The immune response, initiated by C3a, acts by stimulating mast cell degranulation. Inhibiting the binding of C3a to C3aR with antagonists, such as diiminoisoindolines, diminishes the inflammatory response by disrupting the cascade. In many cases, it has been shown to be strong enough to counteract the pro-inflammatory effects of C5a.
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