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Human MIP-1 alpha (CCL3) Recombinant


accession:  P10147
   Size A     5ug   $ 70
   Size B      20ug  $160
   Size C      1mg  $ 2700
Domain  :  IL8
Gene  :  CCL3
Catalog no. :  RKP10147
Optimized DNA sequence encoding Human MIP-1 alpha mature chain was expressed in Escherichia Coli.

Molecular weight:

Native human MIP-1 alpha is generated by the proteolytic removal of the signal peptide. This molecule has a calculated molecular mass of approximately 8 kDa.

Recombinant MIP-1 alpha is a disulfide-linked homodimeric protein consisting of 70 amino acid residue subunits, and migrates as an approximately 8 kDa protein under non-reducing and reducing conditions in SDS-PAGE.

>98%, as determined by SDS-PAGE and HPLC

Biological Activity:
Determined by its ability to chemoattract human monocytes using a concentration range of 1.0-10.0 ng/ml.

Protein Sequence:
        10         20         30         40         50         60 

        70         80         90 
(*)Complete precursor sequence shown, expressed chain highlighted
Endotoxin content was assayed using a LAL gel clot method.
Endotoxin level was found to be less than 0.1 ng/µg(1EU/µg).

Recombinant MIP-1 was lyophilized from a 0.2 μm filtered PBS solution pH 7.5.

A quick spin of the vial followed by reconstitution in distilled water to a concentration not less than 0.1 mg/mL. This solution can then be diluted into other buffers.

The lyophilized protein is stable for at least 2 years from date of receipt at -20° C.
Upon reconstitution, this cytokine can be stored in working aliquots at 2° - 8° C for one month, or at -20° C for six months, with a carrier protein without detectable loss of activity.

Avoid repeated freeze/thaw cycles.

This cytokine product is for research purposes only.It may not be used for therapeutics or diagnostic purposes.



MIP-1 alpha

Macrophage Inflammatory Protein-1 is a factor produced by macrophages that causes local inflammatory responses, and induces superoxide production by neutrophils . Two peptides are responsible for this activity. They have been termed MIP-1-alpha, and MIP- 1-beta. The two MIP proteins are the major factors produced by macrophages following their stimulation with bacterial endotoxins. Both proteins are involved in the cell activation of human granulocytes (neutrophils, eosinophils, and basophils) and appear to be involved in acute neutrophilic inflammation. Both forms of MIP-1 stimulate the production of reactive oxygen species in neutrophils and the release of lysosomal enzymes. They also induce the synthesis of other pro-inflammatory cytokines such as IL1, IL6 and TNF in fibroblasts and macrophages. MIP-1-alpha is a potent agonist of basophils, inducing a rapid change of cytosolic free calcium (see also: Calcium ionophore), the release of histamine and sulfido- leukotrienes, and Chemotaxis. Murine MIP-1- alpha is the primary stimulator of TNF secretion by macrophages, whereas MIP- 1-beta antagonizes the inductive effects of MIP-1- alpha. In human monocytes the production of MIP-1-beta can be induced by bacterial lipopolysaccharides and IL7. The biological activities of MIP-1-alpha and MIP-1-beta are mediated by receptors that bind both factors CCR5. A second species of receptors for these two factors also appears to bind MCAF.

Related Publications:
mip-3 and mip-1 rapidly mobilize dendritic cell precursors into the peripheral blood
J. Leukoc. Biol., Dec 2008; 84: 1549 - 1556.
the role of mip-1 in the development of systemic inflammatory response and organ injury following trauma hemorrhage
J. Immunol., Aug 2008; 181: 2806 - 2812.
free radical production in ca1 neurons induces mip-1 expression, microglia recruitment, and delayed neuronal death after transient forebrain ischemia
J. Neurosci., Feb 2008; 28: 1721 - 1727.
dendritic cell transmigration through brain microvessel endothelium is regulated by mip-1 chemokine and matrix metalloproteinases
J. Immunol., Jan 2007; 178: 520 - 529.
the role of calcium/calmodulin-dependent protein kinase cascade on mip-1 gene expression in atl cells.
Blood (ASH Annual Meeting Abstracts), Nov 2006; 108: 3877.

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