Detects mouse CCL4/MIP-1 beta in Western blots. In this format, less than 1% cross-reactivity with recombinant human (rh) RANTES, rhMIP-1 beta, recombinant mouse (rm) MIP-1 alpha, rhIL-8, rhGRO alpha, rhGRO beta, rhGRO gamma, rhENA‑78, rmMIP‑2, rhMCP‑1, rhMCP-2, rhMCP‑3, rhI-309, rmJE, rmC10, and rhIP-10 is observed.
CCL4/MIP‑1 beta in Mouse Spleen. CCL4/MIP‑1 beta was detected in immersion fixed frozen sections of mouse spleen using Mouse CCL4/MIP‑1 beta Biotinylated Antigen Affinity-purified Polyclonal Antibody (Catalog # BAF451) at 15 µg/mL overnight at 4 °C. Tissue was stained using the Anti-Goat HRP-DAB Cell & Tissue Staining Kit (brown; Catalog # CTS008) and counterstained with hematoxylin (blue). View our protocol for Chromogenic IHC Staining of Frozen Tissue Sections.
Preparation and Storage
Reconstitute at 0.2 mg/mL in sterile PBS.
The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
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 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 downregulation of CCR5 (10). Mature mouse CCL4 shares 77% and 86% aa sequence identity with human 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.
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