Recognizes both recombinant and natural Mouse GRO Beta/CXCL2
Preparations of the factors listed below at 50 ng/mL in a mid-range recombinant mouse CXCL2 control were assayed for interference. No significant interference was observed.
1. 96 well microplate coated with Capture Antibody
2. Detection Antibody conjugated to HRP
4. Wash Buffer Concentrate
5. Dilution Buffer Concentrate
6. Color Reagent A
7. Color Reagent B
8. Stop Solution
This GRO Beta/CXCL2 ELISA Kit, Mouse is an enzyme-linked immunosorbent assay for the quantitative measurement of Mouse GRO Beta/CXCL2 protein in Serum,Cell supernatant . It contains recombinant Mouse GRO Beta/CXCL2, and antibodies raised against the recombinant protein. This ELISA kit is complete and ready-to-use.
This ELISA Kit is shipped at ambient temperature.
Unopened Kit: Store at 2 - 8℃ Opened/Reconstituted Reagents: Please refer to CoA
GRO Beta/CXCL2 ELISA Kit, Mouse: 图片
This standard curve is only for demonstration purposes. A standard curve should be generated for each assay.
This assay recognizes both recombinant and natural Mouse CXCL2. The factors listed below were prepared at 50 ng/mL in dilution buffer and assayed for cross-reactivity. No cross-reactivity was observed.
Chemokine (C-X-C motif) ligand 2 (CXCL2), also called macrophage inflammatory protein 2 (MIP-2), Growth-regulated protein beta (Gro-beta) and Gro oncogene-2 (Gro-2), is a small cytokine belonging to the CXC chemokine family. CXCL2/MIP-2 is selectively up-regulated in tolerance-conferring APCs and serves to recruit NKT cells to the splenic marginal zone, where they form clusters with APCs and T cells. In the absence of the high-affinity receptor for CXCL2/MIP-2 or in the presence of a blocking Ab to CXCL2/MIP-2, peripheral tolerance is prevented, and Ag-specific T regulatory cells are not generated. CXCL2/MIP-2 is selectively up-regulated in tolerance-conferring APCs and serves to recruit NKT cells to the splenic marginal zone, where they form clusters with APCs and T cells. In the absence of the high-affinity receptor for MIP-2 (as in CXCR2-deficient mice) or in the presence of a blocking Ab to MIP-2, peripheral tolerance is prevented, and Ag-specific T regulatory cells are not generated. Understanding the regulation of lymphocyte traffic during tolerance induction may lead to novel therapies for autoimmunity, graft acceptance, and tumor rejection. Several studies have implicated the CXCL2 chemokine as a mediator in the development of sepsis. CXCL2/MIP-2 also plays a major role in mediating the neutrophilic inflammatory response of the rodent lung to particles such as quartz, crocidolite asbestos, as well as high doses of other relative innocuous dusts such as titanium dioxide.