Recombinant Cotton Rat CCL4/MIP‑1 beta (Catalog # 1024-MB)
Measured by its ability to neutralize CCL4/MIP‑1 beta -induced chemotaxis in the BaF3 mouse pro‑B cell line transfected with mouse CCR5. The Neutralization Dose (ND50) is typically 0.4-1.6 µg/mL in the presence of 10 ng/mL Recombinant Cotton Rat CCL4/MIP‑1 beta.
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 CCL4/MIP‑1 beta and Neutralization by Cotton Rat CCL4/MIP‑1 beta Antibody.
Recombinant Cotton Rat CCL4/ MIP‑1 beta (Catalog # 1024‑MB) chemoattracts the BaF3 mouse pro‑B cell line transfected with mouse CCR5 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 Cotton Rat CCL4/MIP‑1 beta (10 ng/mL) is neutralized (green line) by increasing concentrations of Mouse Anti-Cotton Rat CCL4/MIP‑1 beta Monoclonal Antibody (Catalog # MAB1024). The ND50 is typically 0.4‑1.6 µg/mL.
Preparation and Storage
Reconstitute at 0.5 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. *Small pack size (SP) is shipped with polar packs. Upon receipt, store it immediately at -20 to -70 °C
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.
Background: CCL4/MIP-1 beta
CCL4, also known as macrophage inflammatory protein 1 beta (MIP-1 beta ), is a 12 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 (aa) 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 CCR2 (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 down‑regulation of CCR5 (10). Mature cotton rat CCL4 shares 75%‑83% aa sequence identity with human, mouse, and rat CCL4.
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 P. Schmid-Grendelmeier (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.
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