Recombinant Human CCL4/MIP-1 beta Protein, CF Summary
Details of Functionality |
Measured by its ability to chemoattract BaF3 mouse pro‑B cells transfected with human CCR5. The ED50 for this effect is 1‑6 ng/mL. |
Source |
E. coli-derived human CCL4/MIP-1 beta protein Ala24-Asn92 (Major); Pro30-Asn92 (minor) |
Accession # |
|
N-terminal Sequence |
Ala24 (major); Pro30 (minor) |
Protein/Peptide Type |
Recombinant Proteins |
Gene |
CCL4 |
Purity |
>97%, by SDS-PAGE under reducing conditions and visualized by silver stain |
Endotoxin Note |
<0.10 EU per 1 μg of the protein by the LAL method. |
Applications/Dilutions
Dilutions |
|
Theoretical MW |
7.8 kDa (major) & 7.3 kDa (minor). 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. |
Publications |
Read Publications using 271-BME/CF in the following applications:
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Packaging, Storage & Formulations
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.
- 3 months, -20 to -70 °C under sterile conditions after reconstitution.
|
Buffer |
Lyophilized from a 0.2 μm filtered solution in Acetonitrile and TFA. |
Purity |
>97%, by SDS-PAGE under reducing conditions and visualized by silver stain |
Reconstitution Instructions |
Reconstitute at 100 μg/mL in sterile PBS. |
Notes
This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.
Alternate Names for Recombinant Human CCL4/MIP-1 beta Protein, CF
Background
CCL4, also known as macrophage inflammatory protein 1 beta (MIP-1 beta ) is a 7.8 kDa beta chemokine that is secreted at sites of inflammation by activated leukocytes, lymphocytes, vascular endothelial cells, and pulmonary smooth muscle cells (1, 2). CCL4 attracts a variety of immune cells to sites of microbial infection as well as to other pathologic inflammation such as allergic asthma and ischemic myocardium (3 - 8). A CCL4 deficiency in mice promotes the development of autoantibodies, possibly as a result of compromised regulatory T cell recruitment (6). CCL4 is secreted from activated monocytes as a heterodimer with CCL3/MIP-1 alpha (9). The first two N-terminal amino acids can be cleaved from human CCL4 by CD26/DPPIV (10, 11). Both the full length and truncated forms exert biological activity through CCR5, and the truncated form additionally interacts with CCR1 and CCR2b (10). In humans, the ability of CCL4 to bind CCR5 inhibits the cellular entry of M-tropic HIV-1 which utilizes CCR5 as a coreceptor (2). Both forms of CCL4 block HIV-1 infection of T cells by inducing the downregulation of CCR5 (10). Mature human CCL4 shares 77% and 80% aa sequence identity with mouse and rat CCL4, respectively.
- Rot, A. and U.H. von Andrian (2004) Annu. Rev. Immunol. 22:891.
- Menten, P. et al. (2002) Cytokine Growth Factor Rev. 13:455.
- Sun, X. et al. (2006) Infec. Immun. 74:5943.
- Bisset, L.R. and Schmid-Grendelmeier, P. (2005) Curr. Opin. Pulm. Med. 11:35.
- Frangogiannis, N.G. (2004) Inflamm. Res. 53:585.
- Bystry, R.S. et al. (2001) Nat. Immunol. 2:1126.
- Oliveira, S.H.P. et al. (2002) J. Leukoc. Biol. 71:1019.
- Schall, T.J. et al. (1993) J. Exp. Med. 177:1821.
- Guan, E. et al. (2001) J. Biol. Chem. 276:12404.
- Guan, E. et al. (2002) J. Biol. Chem. 277:32348.
- Guan, E. et al. (2004) J. Cell. Biochem. 92:53.
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