Detects mouse CCL9/10/MIP‑1 gamma in ELISAs and Western blots. In sandwich ELISAs, less than 0.02% cross-reactivity with recombinant human CCL3, 4, 15, 19, 20, recombinant mouse CCL3, 4, 19, or recombinant rat CCL20 is observed.
Monoclonal Rat IgG1 Clone # 62105
Protein A or G purified from hybridoma culture supernatant
E. coli-derived recombinant mouse CCL9/10/MIP‑1 gamma Gln22-Gln122 Accession # P51670
Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. *Small pack size (SP) is supplied as a 0.2 µm filtered solution in PBS.
<0.10 EU per 1 μg of the antibody by the LAL method.
Recombinant Mouse CCL9/10/MIP‑1 gamma (Catalog # 463-MG) under non-reducing conditions only
Recombinant Mouse CCL9/10/MIP-1 gamma Protein (Catalog # 463-MG)
Measured by its ability to neutralize CCL9/10/MIP‑1 gamma -induced chemotaxis in the BaF3 mouse pro‑B cell line transfected with human CCR1. The Neutralization Dose (ND50) is typically 1-4 µg/mL in the presence of 0.04 µg/mL Recombinant Mouse CCL9/10/MIP‑1 gamma.
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.
Chemotaxis Induced by CCL9/10/MIP‑1 gamma and Neutralization by Mouse CCL9/10/ MIP‑1 gamma Antibody. Recombinant Mouse CCL9/10/ MIP‑1 gamma (Catalog # 463-MG) chemoattracts the BaF3 mouse pro‑B cell line transfected with human CCR1 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 Mouse CCL9/10/MIP‑1 gamma (0.04 µg/mL) is neutralized (green line) by increasing concentrations of Rat Anti-Mouse CCL9/10/MIP‑1 gamma Monoclonal Antibody (Catalog # MAB463). The ND50 is typically 1-4 µg/mL.
Preparation and Storage
Reconstitute at 0.5 mg/mL in sterile PBS.
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: CCL9/10/MIP-1 gamma
Mouse CCL9/10 (also named MIP-1 gamma and MRP-2) is an 11 kDa, secreted, monomeric polypeptide that belongs to the beta (or CC) intercrine family of chemokines (1‑3). Based on its activity and amino acid (aa) sequence, it is further classified as a member of the NC6 or six cysteine-containing CC subfamily of chemokines (2, 4, 5). This subfamily contains four N-terminally extended chemokines, two human (CCL15 and CCL23) and two mouse (CCL9 and CCL10). Within this subfamily, there are no human-to-rodent interspecies orthologs. Mouse CCL9/10 is synthesized as a 122 aa precursor that contains a 21 aa signal sequence and a 101 aa mature region with six cysteines. As noted, the mature region has an expanded N-terminus relative to other CC family members, and it forms a third intrachain disulfide bond with its two extra cysteines (3‑7). Mouse CCL9/10 is 75% aa identical to rat CCL9/10 (8). Chemokines are known to undergo proteolytic processing to generate multiple isoforms. NC6 chemokines are usually only marginally active at full‑length, but are converted to highly active forms upon N-terminal truncation. Mature CCL9, in the presence of inflammatory fluids, is naturally truncated by 28, 29 or 30 aa at the N-terminus, generating a highly active, 8 kDa, 71‑73 aa CCR1 ligand. In contrast, other CCR1 ligands, CCL3/MIP-1 alpha and CCL5/RANTES, lose their potency when proteolytically processed. CCL9/10 is constitutively secreted, and circulates as a full‑length molecule. Any onset of inflammation with subsequent enzyme release may act on local NC6 chemokines, generating early, potent leukocyte chemoattractants (5, 7).
Zlotnik, A. and O. Yoshie (2000) Immunity 12:121.
Zlotnik, A. et al. (1999) Crit. Rev. Immunol. 19:1
Mohamadzadeh, M. et al. (1996) J. Immunol. 156:3102.
Haelens, A. et al. (1996) Immunobiology 195:499.
Berahovich, R.D. et al. (2005) J. Immunol. 174:7341.
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