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Human CXCL10, amino acids Val22-Pro98 (Accession# NM_001565) was expressed in E. coli.
The 78 amino acid recombinant protein has a predicted molecular mass of approximately 8.7 kD. The DTT-reduced and non-reduced protein migrate at approximately 10 kD by SDS-PAGE. The N-terminal amino acid is Met.
>98%, as determined by Coomassie stained SDS-PAGE.
0.22 µm filtered protein solution is in PBS.
Less than 0.01 ng per µg cytokine as determined by the LAL method.
10-100 µg sizes are bottled at 200 µg/mL. 500 µg and larger sizes are bottled at the concentration indicated on the vial.
Storage & Handling:
Unopened vial can be stored at 4°C for three months, at -20°C for six months, or at -70°C for one year. For maximum results, quick spin vial prior to opening. Stock solutions should be prepared at no less than 10 µg/mL in buffer containing carrier protein such as 1% BSA or HSA or 10% FBS. After dilution, the cytokine can be stored at 4°C for one month or from -20°C to -70°C for up to 3 months. Avoid repeated freeze/thaw cycles.
Bioactivity was measured by its property to chemoattract PHA, IL-2 activated T cells in a dose dependent manner.
CXCL10 is an ELR-negative chemokine structurally and functionally related to CXCL9 and CXCL11. CXCL10, CXCL9, and CXCL11 are produced and secreted by monocytes, macrophages, fibroblasts, and epithelial cells upon stimulation with proinflammatory cytokines, especially IFNγ. CXCL10 chemoattracts CD4, CD8, and NK and NKT cells through the binding to its receptor CXCR3, which is shared with CXCL9 and CXCL11. In addition, CXCL10 inhibits neovascularization in tumors and in wound healing in vivo. Also, CXCL10 has anti-proliferative effects on endothelial cells in vitro, and angiostatic and antitumor effects in vivo. It has been suggested that the anti-proliferative effect of CXCL10 in endothelial cells is CXCR3-independent and that it is mediated through GAG interaction. CXCL10 also possesses antimicrobial activity against E. coli and L. monocytogenes, and both the spore and bacillus forms of B. anthracis. CXCL10 expression is strongly upregulated in many human inflammatory diseases, including rheumatoid arthritis, type I diabetes, multiple sclerosis, atherosclerosis, allograft rejection, and others.
Interferon gamma-stimulated keratinocytes, monocytes, macrophages, fibroblasts, endothelial, T cells
CXCL10 chemoattracts CD4, Th1, CD8, NK, and NKT cells. CXCL10 is induced by inflammatory cytokines, and NH2-terminal cleavage of CXCL10 by DPP-IV/CD26 impairs its chemoattracting capacity and CXCR3 signaling.
Activated T cells, Th1 cells, regulatory T cells, NK cells, NKT cells, endothelial cells, fibroblasts, endothelial cells
1. Luster AD, et al. 1985. Nature 315:672. 2. Loos T, et al. 2008. Blood 112:2648. 3. Crawford MA, et al. 2009. Infect. Immun. 77:1664. 4. Campanella GS, et al. 2010. PLoS One 5:e12700. 5. Hoerning A. 2011. Eur. J. Immunol. 41:2291.
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