All CXCL9 reagents are produced in house and quality controlled, including 10 CXCL9 Antibody, 2 CXCL9 ELISA, 39 CXCL9 Gene, 3 CXCL9 Protein, 2 CXCL9 qPCR. All CXCL9 reagents are ready to use.
Recombinant CXCL9 proteins are expressed by E. coli with fusion tags as Native.
CXCL9antibodies are validated with different applications, which are ELISA, ELISA(Det), WB, IHC-P, ELISA(Cap).
CXCL9cDNA clones are full length sequence confirmed and expression validated. There are 13 kinds of tags for each CXCL9 of different species, especially GFP tag, OFP tag, FLAG tag and so on. There are three kinds of vectors for choice, cloning vector, expression vector and lentivrial expression vector.
CXCL9ELISA Kit are quality controlled by 8 internation QC standard which guarantee every ELISA Kit with high quality.
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.