>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
Endotoxin Note
<0.01 EU per 1 μg of the protein by the LAL method.
Applications/Dilutions
Dilutions
Bioactivity2
Theoretical MW
8.4 kDa. Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
SDS-PAGE
7 kDa, reducing conditions
Publications
Read Publications using 254-XB in the following applications:
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.
3 months, -20 to -70 °C under sterile conditions after reconstitution.
Buffer
Lyophilized from a 0.2 μm filtered solution in PBS containing BSA as carrier protein
Purity
>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
Reconstitution Instructions
Reconstitute at 100 μg/mL in PBS containing at least 0.1% human or bovine serum albumin.
Notes
This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.
Alternate Names for Recombinant Human CXCL5/ENA-78 Protein
chemokine (C-C motif) ligand 5
C-X-C motif chemokine 5
CXCL5
CXCL5/ENA-78
ENA78
ENA-78
ENA-78(1-78)
Epithelial-derived neutrophil-activating protein 78
Neutrophil-activating peptide ENA-78
neutrophil-activating protein 78
SCYB5ENA78
Background
CXCL5, also known as epithelial cell-derived neutrophil-activating peptide (ENA-78), 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 (1-3). 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/GCP-2 and 35%-51% with CXCL1/GRO alpha, CXCL2/GRO beta, CXCL3/GRO gamma, CXCL7/NAP-2, and CXCL8/IL-8. Inflammatory stimulation up-regulates 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 (3-6). Its up-regulation contributes to increased vascularization, tumor growth, and metastasis in many cancers (6-9). Full length CXCL5 (78 aa) is trimmed at the N-terminus by cathepsin G and chymotrypsin to ENA-74 (74 aa) and ENA-70 (70 aa), with the shortened forms showing increased potency relative to full length CXCL5 (10, 11). CXCL5 exerts its effects primarily through interactions with CXCR2 (6, 12). It also binds duffy antigen receptor for chemokines (DARC), which can limit CXCR2-mediated responses (13, 14).
Strieter, R.M. et al. (2005) Cytokine Growth Factor Rev. 16:593.
Balestrieri, M.L. et al. (2008) Cardiovasc. Res. 78:250.
Walz, A.. et al. (1991) J. Exp. Med. 174:1355.
Strieter, R.M. et al. (1992) Immunol. Invest. 21:549.
Koch, A.E. et al. (1994) J. Clin. Invest. 94:1012.
Begley, L.A. et al. (2008) Neoplasia 10:244.
Vandercappellen, J. et al. (2008) Cancer Lett. 267:226.
Arenberg, D.A. et al. (1998) J. Clin. Invest. 102:465.
Miyazaki, H. et al. (2006) Cancer Res. 66:4279.
Wuyts, A. et al. (1999) Eur. J. Biochem. 260:421.
Nufer, O. et al. (1999) Biochemistry 38:636.
Ahuja, S.K. and P.M. Murphy (1996) J. Biol. Chem. 271:20545.
Kashiwazaki, M. et al. (2003) Int. Immunol. 15:1219.
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