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Human MIP-1 beta (CCL4) Recombinant

MIP-1

accession:  P13236
   Size A     2ug   $ 70
   Size B      10ug  $160
   Size C      1mg  $ 2700
Domain  :  IL8
Gene  :  CCL4
Catalog no. :  RKP13236
Source:
Optimized DNA sequence encoding Human MIP-1 beta chain was expressed in Escherichia Coli.

 
Molecular weight:

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

Recombinant MIP-1 beta  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.


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

 
Biological Activity:
Determined by its ability to chemoattract human blood monocytes using a concentration range of 2.0-10.0 ng/ml.

 
Protein Sequence:
        10         20         30         40         50         60 
MKLCVTVLSL LMLVAAFCSP ALSAPMGSDP PTACCFSYTA RKLPRNFVVD YYETSSLCSQ 

        70         80         90 
PAVVFQTKRS KQVCADPSES WVQEYVYDLE LN 
(*)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 MIP-1 beta 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.

 

MIP-1 beta

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:
an arrestin-dependent multi-kinase signaling complex mediates mip-1/ccl4 signaling and chemotaxis of primary human macrophages
J. Leukoc. Biol., Jul 2009; 10.1189/jlb.0908551.
role of mip-1β in a mouse model of oxygen induced retinopathy
Invest. Ophthalmol. Vis. Sci., Apr 2009; 50: 4138.
highly potent hiv inhibition: engineering a key anti-hiv structure from psc-rantes into mip-1β/ccl4
Protein Eng. Des. Sel., Feb 2008; 21: 65 - 72.
elevated levels of il-17, mip-1 ß, mig and itac in b-cell chronic lymphocytic leukemia: correlation with prognostic markers.
Blood (ASH Annual Meeting Abstracts), Nov 2006; 108: 2788.
suppression of mip-1ß transcription in human t cells is regulated by inducible camp early repressor (icer)
J. Leukoc. Biol., Feb 2006; 79: 378 - 387.




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