Measured by its ability to neutralize CXCL5/ENA‑78-induced chemotaxis in the BaF3 mouse pro‑B cell line transfected with human CXCR2. The Neutralization Dose (ND50) is typically 4-16 µg/mL in the presence of 30 ng/mL Recombinant Human CXCL5/ENA‑78.
Please Note: Optimal dilutions should be determined by each laboratory for each application.
are available in the Technical Information section on our website.
Chemotaxis Induced by CXCL5/ENA‑78 and Neutralization by Human CXCL5/ ENA‑78 Antibody.
Recombinant Human CXCL5/ENA‑78 (Catalog # 254‑XB) chemoattracts the BaF3 mouse pro‑B cell line transfected with human CXCR2 in a dose-dependent manner (orange line). The amount of cells that migrated through to the lower chemotaxis chamber was measured by Resazurin (Catalog # AR002). Chemotaxis elicited by Recombinant Human CXCL5/ ENA‑78 (30 ng/mL) is neutralized (green line) by increasing concentrations of Goat Anti-Human CXCL5/ ENA‑78 Polyclonal Antibody (Catalog # AB-254-PB). The ND50 is typically 4-16 µg/mL.
Preparation and Storage
Reconstitute at 1 mg/mL in sterile PBS.
Reconstitution Buffer Available
The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
Stability & Storage
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70 °C as supplied.
1 month, 2 to 8 °C under sterile conditions after reconstitution.
6 months, -20 to -70 °C under sterile conditions after reconstitution.
CXCL5, also known as epithelial cell-derived-neutrophil-activating-peptide (ENA78), is an 8 kDa proinflammatory member of the CXC subfamily of chemokines. Its Glu-Leu-Arg (ELR) motif confers angiogenic properties and distinguishes it from ELR- CXC chemokines which are angiostatic. Human CXCL5 shares 57% amino acid (aa) sequence identity with mouse and rat CXCL5. Among other human ELR+ chemokines, it shares 77% aa sequence identity with CXCL6/GCP2 and 35%‑51% with CXCL1/GRO alpha, CXCL2/GRO beta, CXCL3/GRO gamma, CXCL7/NAP2, and CXCL8/IL8. Inflammatory stimulation upregulates CXCL5 production in multiple hematopoietic cell types, fibroblasts, endothelial cells, and vascular smooth muscle cells. In vivo, CXCL5 is elevated at sites of inflammation and pulmonary fibrosis where it promotes neutrophil infiltration and activation as well as angiogenesis. Its upregulation contributes to increased vascularization, tumor growth, and metastasis in many cancers. Full length CXCL5 (78 aa) is trimmed at the N-terminal end by Cathepsin G and chymotrypsin to ENA74 (74 aa) and ENA70 (70 aa), with the shortened forms showing increased potency relative to full length CXCL5. CXCL5 exerts its effects primarily through interactions with CXCR2. It also binds DARC, a decoy chemokine receptor which can limit CXCR2-mediated responses.
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