Mouse CXCL1/GRO alpha/KC/CINC-1 Biotinylated Antibody

KC, a member of the alpha (CXC) chemokine subfamily, was initially identified as an immediate early gene induced in mouse fibroblasts by platelet-derived growth factor. KC cDNA encodes a 96 amino acid (aa) residue precursor protein with a predicted secretory signal peptide that is removed to yield the mature protein. The protein sequence of mouse KC shows approximately 63% identity to that of mouse MIP-2. KC is also approximately 60% identical to the human GROs. It has been suggested that mouse KC and MIP-2 are the orthologs of the human GROs and rat CINCs. In addition to mouse fibroblasts, KC is expressed in macrophages and endothelial cells. Mouse KC is a potent neutrophil attractant and activator. The functional receptor for KC has been identified as CXCR2. Based on the pattern of KC expression in a number of inflammatory disease models, KC appears to have an important role in inflammation. KC was found to be involved in monocyte arrest on atherosclerotic endothelium and may also play a pathophysiological role in Alzheimer’s disease. Many chemokines are substrates for selective proteolysis at the amino-terminus by various proteases including dipeptidyl peptidase IV or matrix metalloproteases, resulting in truncated chemokine isoforms with different (both enhanced or reduced) bioactivities. The naturally occurring 68 aa N-terminal truncated isoform of mouse KC is reported to be a more potent synergistic growth stimulants for CFU-GM. As a chemoattractant for hCXCR2 transfected mouse Baf/3 cells, the truncated form of mouse KC (aa 29-96) is also approximately 5-fold more active than 77 aa residue form of KC (aa 20-96, R&D Systems, Catalog # 453-KC) (1-4).