This mouse IgG2a monoclonal antibody [5G9] was generated against human C3b-sepharose and reacts with human and primate complement component 3b (C3b) and iC3b; blocks activation of the classical pathway of complement.
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.
|Immunogen:||Human C3b -Sepharose|
|Epitope:||Human complement component 3b (C3b) and iC3b|
|Purification Method:||Protein G Affinity|
|Buffer:||0.1M Sodium Phosphate, pH 7.4, 0.15M NaCl, 0.05% (w/v) Sodium Azide|
|Tested Applications:||Neutralizing and Flow Cytometry|
|Comments:||5G9 blocks activation of the classical pathway of complement|
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