Anti-Human MIP-1α

Purified Recombinant Human MIP-1α (>98%)

This antigen affinity purified polyclonal antibody has been 0.2 µm filtered and lyophilized from modified Dulbecco’s phosphate buffered saline (1X PBS) pH 7.2 – 7.3 containing 5.0% w/v trehalose with no calcium, magnesium, or preservatives present.

Lyophilized

The lyophilized antigen affinity purified polyclonal antibody can be stored desiccated at -20°C to -70°C for twelve months from date of receipt. The reconstituted antibody can be stored for at least four weeks at 2-8°C. For long-term storage of the reconstituted antibody, aseptically aliquot into working volumes and store at -20°C to -70°C in a manual defrost freezer. Avoid Repeated Freeze Thaw Cycles. No detectable loss of activity was observed after six months.

Next Day Ambient

Immunohistochemistry: Suitable for use at concentration of 5-15 µg/mL.
Neutralization: Measured by its ability to neutralize CCL3/MIP‑1 alpha -induced chemotaxis in the BaF3 mouse pro‑B cell line transfected with human CCR5. The Neutralization Dose (ND₅₀) is typically 2-8 µg/mL in the presence of 0.1 µg/mL Recombinant Human CCL3/MIP‑1 alpha isoform LD78a.

Goat Anti-Human Macrophage Inflammatory Protein 1 Alpha (MIP-1α) recognizes Human MIP-1α. This antigen affinity purified polyclonal antibody was purified using a proprietary chromatographic technique that includes covalently immobilizing the antigen proteins or peptides to agarose based beads. This purification method enhances specificity, reduces nonspecific binding of extraneous IgG and provides you with the most reliable reagent available for your early discovery research.

Macrophage inflammatory protein 1 alpha (MIP-1 alpha) is a potent inhibitor of hemopoietic stem cell proliferation and is a member of a family of pro- inflammatory mediators, the chemokine family.¹ MIP-1 alpha is a particularly interesting chemokine, because in addition to its proinflammatory activities, it inhibits the proliferation of hematopoietic stem cells.² The role of MIP-1 alpha seems to be related to production of TNF-alpha, which in turn up-regulates vascular adhesion molecules required for neutrophil influx.³

1. Pragnel, IB. et al. (1994) J. Biol. Chem. 269: 4974
2. Cook, DN. et al. (1996) J. of Leukocyte Biol. 59: 61
3. Ward, PA. et al. (1995) J of Immunol. 154: 4793