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Mouse MIP-1gamma (CCL9) Recombinant

MIP-1

accession:  P51670
   Size A     5ug   $ 70
   Size B      20ug  $160
   Size C      1mg  $ 2700
Domain  :  IL8
Gene  :  CCL9
Catalog no. :  RKP51670
Source:
Optimized DNA sequence encoding mouse MIP-1 gamma chain was expressed in Escherichia Coli.

 
Molecular weight:

Native mouse MIP-1gamma (CCL9) is generated by the proteolytic removal of the signal peptide and propeptide. This molecule has a calculated molecular mass of approximately 12 kDa.

Recombinant CCL9  is a disulfide-linked homodimeric protein consisting of  102 amino acid residue subunits, and migrates as an approximately 12 kDa protein under non-reducing and reducing conditions in SDS-PAGE.


 
Purity:
>95%, as determined by SDS-PAGE and HPLC

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

 
Protein Sequence:
        10         20         30         40         50         60 
MKPFHTALSF LILTTALGIW AQITHATETK EVQSSLKAQQ GLEIEMFHMG FQDSSDCCLS 

        70         80         90        100        110        120 
YNSRIQCSRF IGYFPTSGGC TRPGIIFISK RGFQVCANPS DRRVQRCIER LEQNSQPRTY 


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

 
Presentation:
Recombinant CCL9 was lyophilized from a 0.2 μm filtered PBS solution.

 
Reconstitution:
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

 
Storage:
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.

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

 

CCL9

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:
icsbp-mediated immune protection against bcr-abl–induced leukemia requires the ccl6 and CCL9 chemokines
Blood, Apr 2009; 113: 3813 - 3820.
the cxcl12, periostin, and CCL9 genes are direct targets for early b-cell factor in op-9 stroma cells
J. Biol. Chem., May 2007; 282: 14454 - 14462.
chemokine and chemokine receptor expression during colony stimulating factor-1–induced osteoclast differentiation in the toothless osteopetrotic rat: a key role for CCL9 (mip-1) in osteoclastogenesis in vivo and in vitro
Blood, Mar 2006; 107: 2262 - 2270.




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