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CXCL9 / MIG Protein, Antibody, ELISA Kit, cDNA Clone

CXCL9 / MIG Related Areas

CXCL9 / MIG Related Pathways

CXCL9 / MIG Related Protein, Antibody, cDNA Gene, and ELISA Kits

CXCL9 / MIG Summary & Protein Information

CXCL9 / MIG Related Information

CXCL9 / MIG Background

Gene Summary: The function of CXCL9 gene has not been specifically defined; however, it is thought to be involved in T cell trafficking. CXCL9 gene has been localized to 4q21 with INP10, which is also a member of the chemokine family of cytokines. [provided by RefSeq, Jul 2008]
General information above from NCBI
Subcellular location: Secreted.
Induction: By IFNG/IFN-gamma. The induction is enhanced by TNF in dermal fibroblasts and vein endothelial cells.
Sequence similarity: Belongs to the intercrine alpha (chemokine CxC) family.
General information above from UniProt

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.

CXCL9 / MIG Alternative Name

CMK,MIG,Humig,SCYB9,crg-10, [homo-sapiens]
CMK,crg-10,CXCL9,Humig,MIG,SCYB9, [human]
crg-10,Cxcl9,Mig,MuMIG,Scyb9,BB139920,CMK, [mouse]
CMK,Mig,MuMIG,Scyb9,crg-10,BB139920, [mus-musculus]

CXCL9 / MIG Related Studies

  • 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.