>97%, by SDS-PAGE under reducing conditions and visualized by silver stain.
Endotoxin Note
<0.01 EU per 1 μg of the protein by the LAL method.
Applications/Dilutions
Dilutions
Bioactivity
Theoretical MW
7.8 kDa. Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
Publications
Read Publications using 451-MB in the following applications:
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.
3 months, -20 to -70 °C under sterile conditions after reconstitution.
Buffer
Lyophilized from a 0.2 μm filtered solution in Acetonitrile and TFA with BSA as a carrier protein.
Purity
>97%, by SDS-PAGE under reducing conditions and visualized by silver stain.
Reconstitution Instructions
Reconstitute at 100 μg/mL in sterile PBS containing at least 0.1% human or bovine serum albumin.
Notes
This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.
Alternate Names for Recombinant Mouse CCL4/MIP-1 beta Protein
ACT2
ACT-2
AT744.1
C-C motif chemokine 4
CCL4
chemokine (C-C motif) ligand 4
Exodus-3
G-26 T-lymphocyte-secreted protein
G-26
HC21
LAG1
LAG-1
Lymphocyte activation gene 1 protein
Macrophage inflammatory protein 1-beta
MIP1 beta
MIP-1 beta
MIP1B
MIP1B1
MIP-1-beta
MIP-1-beta(1-69)
PAT 744
Protein H400
SCYA2
SCYA4
secreted protein G-26
SIS-gamma
small inducible cytokine A4 (homologous to mouse Mip-1b)
Small-inducible cytokine A4
T-cell activation protein 2
Background
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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