Human CCL4/MIP-1 beta Antibody Summary
Ala24-Asn92
Accession # P13236
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Scientific Data
Chemotaxis Induced by CCL4/MIP‑1 beta and Neutralization by Human CCL4/MIP‑1 beta Antibody. Recombinant Human CCL4/MIP-1 beta (Catalog # 271-BME) chemoattracts the BaF3 mouse pro-B cell line transfected with human CCR5 in a dose-dependent manner (orange line). The amount of cells that migrated through to the lower chemotaxis chamber was measured by Resazurin. Chemotaxis elicited by Recombinant Human CCL4/MIP-1 gamma (5 ng/mL) is neutralized (green line) by increasing concentrations of Human CCL4/MIP-1 gamma Polyclonal Antibody (Catalog # AB-271-NA). The ND50 is typically 1.5-9 µg/mL.
Reconstitution Calculator
Preparation and Storage
- 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.
Background: CCL4/MIP-1 beta
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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