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Human CXCL9, amino acids Thr23 – Thr125 (Accession # NM_002416.1) was expressed in E. coli.
The 103 amino acid recombinant protein has a predicted molecular mass of approximately 11.7 kD. The DTT-reduced protein migrates at approximately 15 kD, and the non-reduced protein migrates at approximately 18 kD by SDS-PAGE. The N-terminal amino acid is Threonine.
>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 human T cells activated with PHA and IL-2 in a dose dependent manner.
CXCL9 is an inflammatory chemokine initially identified by differential screening of a cDNA library from lymphokine-activated macrophages. CXCL9 is a CXC chemokine and member of the non-ELR (lacking a Glu-Leu-Arg motif in the N-terminal region) CXC chemokine family. CXCL9 shares the CXCR3 receptor with CXCL10 and CXCL11, and these ligands differ in their receptor-binding and -activating properties; CXCL11 is more potent than CXCL10, and CXCL10 is more potent than CXCL9. An alternative spliced variant, CXCR3B, has been described for CXCR3. CXCR3B mediates the angiostatic effect of CXCR3 ligands and is the receptor for PF4 (CXCL4). CXCR3B has been detected in human neoplastic tissues. CXCL9 plays a key role in leukocyte trafficking, acting on activated CD4+ Th1 cells, CD8+ T cells, IL-2 activated T lymphocytes, and NK cells. Also, CXCL9 (as well as CXCL10 and CXCL11) induces angiostatic effects in human microvacular endothelial cells. In addition, CXCL9 enhances T lymphocyte function in alloimmune response; CXCL9 induces T cells proliferation and cytokine production in an experimental model of cardiac allograft vasculopathy. CXCL9 is induced by cytokines, particularly IFNγ during infection, injury, or immunoinflammatory responses, and it can be inactivated by CD26/dipeptidil peptidase IV after truncation by this protease. Amino-terminal truncation of CXCL9 by CD26 impairs lymphocyte chemotaxis, but the antiangiogenic activity is not affected. In rheumatoid arthritis, CXCL9 is synergistically stimulated by TNFα or IL-1a and IFNγ.
Monokine induced by interferon gamma (MIG); Small inducible cytokine, subfamily B, member 9 (SCYB9)
CXCL9 is secreted by monocytes, macrophages, APC, eosinophils, endothelial cells, and B cells. Also, CXCL9 is secreted by fibroblasts in inflammatory conditions.
CXCL9 plays a key role in leukocyte trafficking, acting on activated CD4+ Th1 cells, CD8+ T cells, IL-2 activated T lymphocytes, and NK cells. Also, CXCL9 (as well as CXCL10 and CXCL11) induces angiostatic effects in human microvacular endothelial cells.
1. Loetscher M, et al. 1996. J. Exp. Med. 184:963. 2. Lambeir AM, et al. 2001. J. Biol. Chem. 276:29839. 3. Lasagni L, et al. 2003. J. Exp. Med. 197:1537. 4. Whiting D, et al. 2004. J. Immunol. 172:7417. 5. Proost P, et al. 2004. J. Leuko. Biol. 75:777. 6. Gorbachev AV, et al. 2007. J. Immunol. 178: 2278. 7. Rosenblum JM, et al. 2010. J. Immunol. 184:3450. 8. Crawford MA, et al. 2010. PLoS Pathog. 6:e1001199.
Recombinant Human CXCL9 (MIG) (carrier-free), Recombinant, CXCL9 recombinant protein, recombinant CXCL9 protein, Monokine induced by interferon gamma (MIG); Small inducible cytokine, subfamily B, member 9 (SCYB9), Bioassay (Recombinants), Immunology, Antibodies
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