E. coli-derived recombinant mouse CXCL1/KC Arg20-Lys96 Accession # P12850
Specificity
Detects mouse CXCL1/GRO alpha /KC/CINC-1 in ELISAs and Western blots. In sandwich immunoassays, less than 40% cross-reactivity with recombinant rat (rr) CINC-1 is observed and less than 0.05% cross-reactivity with rrCINC-2 alpha , rrCINC-2 beta , recombinant mouse (rm) CRG-2, rmMIG, and rmMIP-2 is observed.
Source
N/A
Isotype
IgG
Clonality
Polyclonal
Host
Goat
Gene
Cxcl1
Purity Statement
Antigen Affinity-purified
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Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70 °C as supplied.
1 month, 2 to 8 °C under sterile conditions after reconstitution.
6 months, -20 to -70 °C under sterile conditions after reconstitution.
Buffer
Lyophilized from a 0.2 μm filtered solution in PBS with BSA as a carrier protein.
Preservative
No Preservative
Concentration
LYOPH
Reconstitution Instructions
Reconstitute at 0.2 mg/mL in sterile PBS.
Notes
This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.
Alternate Names for CXCL1/GRO alpha/KC/CINC-1 Antibody [Biotin]
CINC1
CINC-1
CXCL1
FSP
GRO alpha
GRO1
GROa
KC
MGSA
MGSA-a
MGSA-alpha
NAP-3
SCYB1
Background
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).
King, A.G. et al. (2000) J. Immunol. 164:3774.
Oquendo, P. et al. (1989) J. Biol. Chem. 264:4133.
Huo, Y. et al. (2001) J. Clin. Invest. 108:1307.
Xia, M. et al. (2002) J. Neuroimmunol. 122:55.
Limitations
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.
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