Human CXCL9/MIG ELISA Kit | CXCL9/MIG elisa kit

Human CXCL9/MIG ELISA Kit

Cat. Num. AAA258400

• Reactivity: Human
• Synonyms: CXCL9/MIG; N/A; Human CXCL9/MIG ELISA Kit; MIG/CXCL9 ELISA Kit, Human; chemokine (C-X-C motif) ligand 9; CMK ELISA Kit, Human; crg-10 ELISA Kit, Human; Humig ELISA Kit, Human; MIG ELISA Kit, Human; SCYB9 ELISA Kit, Human; CXCL9/MIG elisa kit

• Reactivity: Human
• Specificity: For the quantitative determination of Human CXCL9/MIG concentration in serum.
• Assay Type: Solid Phase Sandwich ELISA (quantitative)
• Sample Types: Serum
• Detection Range: 6.25-400pg/mL
• Sensitivity: 1.47pg/mL
• Conjugation: HRP
• Materials Provided: 1. 96 well microplate coated with Capture Antibody; 2. Detection Antibody conjugated to HRP; 3. Standards; 4. Wash Buffer Concentrate; 5. Dilution Buffer Concentrate; 6. Color Reagent A; 7. Color Reagent B; 8. Stop Solution

Application Data

(This assay recognizes both recombinant and natural human CXCL9. The factors listed below were prepared at 50ng/mL in dilution buffer and assayed for cross-reactivity. No cross-reactivity was observed.)

Standard Curve (Sample)

(This standard curve is only for demonstration purposes. A standard curve should be generated for each assay.)

Related Product Information for CXCL9/MIG elisa kit

This MIG/CXCL9 ELISA Kit, Human is an enzyme-linked immunosorbent assay for the quantitative measurement of Human MIG/CXCL9 protein in Serum. It contains recombinant Human MIG/CXCL9, and antibodies raised against the recombinant protein. This ELISA kit is complete and ready-to-use.

Background: Chemokine (C-X-C motif) ligand 9 (CXCL9), also known as Monokine induced by gamma interferon (MIG), is a small cytokine belonging to the CXC chemokine family. The function of this chemokine has not been specifically defined; however, it is thought to be involved in T cell trafficking. CXCL9/MIG functions as one of the three ligands of chemokine receptor CXCR3 which is a G protein-coupled receptor found predominantly on T cells. CXCL9/MIG, together with CXCL10 and CXCL11, may activate CXCR3 by binding to it. CXCL9 serves as a cytokine that affects the growth, movement, or activation state of cells that participate in immune and inflammatory response. It has been observed that tumour endothelial cells secrete high levels of CXCL9 in all, and CXCL10 in most melanoma metastases. Experiment data represent novel mechanisms by which tumour cells in melanoma metastases might use the chemokine-expressing endothelium to leave the tumour and eventually to form additional metastases at distinct sites. Experiment results also improved that CXCL9/MIG plays an important role in CD4+ T lymphocyte recruitment and development of CAV, MOMA-2+ macrophages are the predominant recipient-derived source of CXCL9/MIG, and recipient CD4 lymphocytes are necessary for sustained CXCL9/MIG production and CAV development in this model. Neutralization of the chemokine CXCL9/MIG may have therapeutic potential for the treatment of chronic rejection after heart transplantation.

References

Ruehlmann JM, et al. (2001) MIG (CXCL9) chemokine gene therapy combines with antibody-cytokine fusion protein to suppress growth and dissemination of murine colon carcinoma. Cancer Res. 61(23): 8498-503.
Belperio JA, et al. (2003) Role of CXCL9/CXCR3 chemokine biology during pathogenesis of acute lung allograft rejection. J Immunol. 171(9): 4844-52.
Colvin RA, et al. (2004) Intracellular domains of CXCR3 that mediate CXCL9, CXCL10, and CXCL11 function. J Biol Chem. 279(29): 30219-27.
Valbuena G, et al. (2003) Expression analysis of the T-cell-targeting chemokines CXCL9 and CXCL10 in mice and humans with endothelial infections caused by rickettsiae of the spotted fever group. Am J Pathol. 163(4): 1357-69.