Anti-Complement C3b-iC3b [3E7] Antibody
![Anti-Complement C3b-iC3b [3E7] Antibody](https://www.kerafast.com/MediaStorage/Product/Images/Large/1015_2001202001263110140.jpg "Anti-Complement C3b-iC3b [3E7] Antibody")
This mouse IgG1 monoclonal antibody [3E7] was generated against human C3b and reacts with human and primate complement component 3b (C3b) and iC3b; blocks activation of the alternative pathway of complement.
Highlights
- Reacts with both human and primate C3b and iC3b
- Blocks activation of the alternative pathway of complement
- Suitable for Western Blot, Immunohistochemistry and Neutralizing applications
The complement system consists of a number of small proteins found in the blood, generally synthesized by the liver, and normally circulating as inactive precursors (pro-proteins). When stimulated by one of several triggers, proteases in the system cleave specific proteins to release cytokines and initiate an amplifying cascade of further cleavages. The end-result of this activation cascade is massive amplification of the response and activation of the cell-killing membrane attack complex.
Complement component 3 (C3) plays a central role in the activation of the complement system. C3 cleavage by C3-convertase produces C3b and iC3b. C3b leads to an inflammatory response and also covalently binds to microbial cell surfaces aiding in opsonization of the microbe.
From the laboratory of Ronald P. Taylor, PhD, University of Virginia
Part of The Investigator's Annexe program.
This mouse IgG1 monoclonal antibody [3E7] was generated against human C3b and reacts with human and primate complement component 3b (C3b) and iC3b; blocks activation of the alternative pathway of complement.
Highlights
- Reacts with both human and primate C3b and iC3b
- Blocks activation of the alternative pathway of complement
- Suitable for Western Blot, Immunohistochemistry and Neutralizing applications
The complement system consists of a number of small proteins found in the blood, generally synthesized by the liver, and normally circulating as inactive precursors (pro-proteins). When stimulated by one of several triggers, proteases in the system cleave specific proteins to release cytokines and initiate an amplifying cascade of further cleavages. The end-result of this activation cascade is massive amplification of the response and activation of the cell-killing membrane attack complex.
Complement component 3 (C3) plays a central role in the activation of the complement system. C3 cleavage by C3-convertase produces C3b and iC3b. C3b leads to an inflammatory response and also covalently binds to microbial cell surfaces aiding in opsonization of the microbe.
From the laboratory of Ronald P. Taylor, PhD, University of Virginia
Part of The Investigator's Annexe program.
| Product Type: | Antibody |
| Antigen: | C3b |
| Accession ID: | P01024 |
| Isotype: | IgG1 |
| Clonality: | Monoclonal |
| Clone Name: | 3 E7 |
| Reactivity: | Primate, Human |
| Immunogen: | Human C3b |
| Species Immunized: | Mouse |
| Purification Method: | Protein G Affinity |
| Buffer: | 0.1M Sodium Phosphate, pH 7.4, 0.15M NaCl, 0.05% (w/v) Sodium Azide |
| Tested Applications: | IHC, WB, Neutralizing |
| Comments: | 3E7 blocks activation of the alternative pathway of complement |
| Storage: | -20C |
| Shipped: | Cold packs |
- Lindorfer MA, Pawluczkowycz AW, Peek EM, Hickman K, Taylor RP, Parker CJ. A novel approach to preventing the hemolysis of paroxysmal nocturnal hemoglobinuria: both complement-mediated cytolysis and C3 deposition are blocked by a monoclonal antibody specific for the alternative pathway of complement. Blood. 2010 Mar 18;115(11):2283-91.
- DiLillo DJ, Pawluczkowycz AW, Peng W, Kennedy AD, Beum PV, Lindorfer MA, Taylor RP. Selective and efficient inhibition of the alternative pathway of complement by a mAb that recognizes C3b/iC3b. Mol Immunol. 2006 Mar;43(7):1010-9.
- Kennedy AD, Solga MD, Schuman TA, Chi AW, Lindorfer MA, Sutherland WM, Foley PL, Taylor RP. An anti-C3b(i) mAb enhances complement activation, C3b(i) deposition, and killing of CD20+ cells by rituximab. Blood. 2003 Feb 1;101(3):1071-9.
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