This monoclonal antibody reacts with natural and recombinant human MCP-1. Does not react with human interleukin-8 (IL-8) and other human cytokines tested such as interleukin-1ß (IL-1ß), serum amyloid A (SAA) and epidermal growth factor (EGF).
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
ELISA: Use at an assay dependent dilution.
Neut: Use at a concentration of 0.5 µg/ml.
WB: Use at a concentration of 0.1 - 1 µg/ml. Predicted molecular weight: 11 kDa.
Not tested in other applications.
Optimal dilutions/concentrations should be determined by the end user.
This antibody can be used as a capture antibody in sandwich ELISA applications for human MCP-1 detection in combination with a monoclonal tracer/detection antibody (HRP-conjugated or biotin-conjugated). Suggested Capture Coating Dose: 0.3µg/well; Substrate: TMB. If the above suggested conditions are followed approximately 1.5 pg/mL of MCP-1 in serum/plasma or 4 pg/mL of MCP-1 in medium can be detected with an assay range of 0-1600 pg/mL.
Tests on the ability to inhibit monocyte chemotaxis toward 1 nM recombinant human MCP-1 in blindwell chambers showed that the antibodies were particularly effective at blocking MCP-1 activity at a concentration of 0.5µg/mL. It was also found that S-14 could inhibit the function of native MCP-1 at concentrations similar to inhibitory doses for recombinant MCP-1.
Concentration of 0.1-1.0 µg/mL will allow visualization of 0.1 µg/lane of human MCP-1
Chemotactic factor that attracts monocytes and basophils but not neutrophils or eosinophils. Augments monocyte anti-tumor activity. Has been implicated in the pathogenesis of diseases characterized by monocytic infiltrates, like psoriasis, rheumatoid arthritis or atherosclerosis. May be involved in the recruitment of monocytes into the arterial wall during the disease process of atherosclerosis.
Belongs to the intercrine beta (chemokine CC) family.
Processing at the N-terminus can regulate receptor and target cell selectivity. Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant.
Liu M et al. Molecular Mechanisms of Stress-Induced Myocardial Injury in a Rat Model Simulating Posttraumatic Stress Disorder. Psychosom Med78:888-895 (2016).
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Sardo MA et al. Tissue factor and monocyte chemoattractant protein-1 expression in hypertensive individuals with normal or increased carotid intima-media wall thickness. Clin Chem54:814-23 (2008).
Read more (PubMed: 18339698) »