Chemotaxis Induced by CCL11/Eotaxin and Neutralization by Mouse CCL11/Eotaxin Antibody. Recombinant Mouse CCL11/|
Eotaxin (Catalog # 420‑ME) chemoattracts the Y3 rat myeloid cell line transfected with human CCR3 in a dose-dependent manner (orange line). The amount of cells that migrated through to the lower chemotaxis chamber was measured by MTT staining. Chemotaxis elicited by Recombinant Mouse CCL11/
Eotaxin (0.1 µg/mL) is neutralized (green line) by increasing concentrations of Rat Anti‑Mouse CCL11/Eotaxin Monoclonal Antibody (Catalog # MAB420). The ND50 is typically 3‑30 µg/mL.
|CCL11/Eotaxin in Rat Intestine. CCL11/Eotaxin was detected in perfusion fixed frozen sections of rat intestine using Rat Anti-Mouse CCL11/Eotaxin Monoclonal Antibody (Catalog # MAB420) at 15 µg/mL overnight at 4 °C. Tissue was stained using the Anti-Rat HRP-DAB Cell & Tissue Staining Kit (brown; Catalog # CTS017) and counterstained with hematoxylin (blue). Specific staining was localized to fibroblasts in submucosae. View our protocol for Chromogenic IHC Staining of Frozen Tissue Sections.|
CCL11 is a potent eosinophil chemoattractant that was originally purified from bronchoalveolar lavage fluid of guinea pigs sensitized by aerosol challenge with ovalbumin. Mouse CCL11 cDNA encodes a 97 amino acid (aa) precursor protein from which the amino-terminal 23 aa are cleaved to generate the 74 aa mature mouse CCL11. At the protein sequence level, mature mouse CCL11 is approximately 60% identical to mature human and guinea pig CCL11. In addition, mouse CCL11 also shows high aa sequence identity to members of the MCP family. Mouse CCL11 is chemotactic for eosinophils, but not mononuclear cells or neutrophils. CCL11 mRNA is expressed in a variety of tissues. The expression of CCL11 mRNA is induced in cultured endothelial cells in response to IFN-gamma. In addition, CCL11 mRNA is also induced in response to the transplantation of IL-4-secreting tumor cells. The CC chemokine receptor 3 (CCR3) has been identified as a specific human CCL11 receptor.
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