Anti-MICA/MICB FITC (Clone : 6D4)
Figure 1 : Separation of Jurkat cells stained using anti-human MICA/MICB (6D4) FITC antibody (concentration in sample 5 µg/ml, red-filled) from unstained Jurkat cells (black-dashed) in flow cytometry analysis (surface staining).
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Amount : | 0.1 mg |
Isotype : | Mouse IgG2a |
Purification : | The purified antibody is conjugated with fluorescein isothiocyanate (FITC) under optimum conditions. The conjugate is purified by size-exclusion chromatography. |
Content : | 1 mg/ml Formulation : Stabilizing phosphate buffered saline (PBS) solution containing 15 mM sodium azide |
Storage condition : | Store in the dark at 2-8°C. Do not freeze. Avoid prolonged exposure to light. |
Immunogen Information : | Transfected C1R cells expressing MICA |
MICA and MICB glycoproteins are members of MHC class I family, closely linked to HLA-B. However, unlike HLA molecules, MICA and MICB are not associated with beta2 microglobulin and are conformationally stable in the absence of conventional MHC class I peptide ligands. Both proteins are stress-induced antigens expressed mainly in gastrointestinal epithelium, where they are recognized by V-delta1 subset of gamma/delta T cells, and also on diverse epithelial tumor cells. Binding of MICA/MICB receptor, the NKG2D, leads to cytolytic response of NK cells, Tc cells, and gamma/delta T cells. Alternative splicing results in multiple isoforms, and some of them have been associated with susceptibility to psoriasis and psoriatic arthritis. Shedding of MICA-related antibodies and ligands is involved in the progression from monoclonal gammopathy of undetermined significance to multiple myeloma.
Specificity : The mouse monoclonal antibody 6D4 recognizes a common extracellular epitope on MICA and MICB glycoproteins, transmembrane ligands of NKG2D, and is able to block NKG2D-mediated activation of NK cells and cytotoxic T cells.
Specificity : The mouse monoclonal antibody 6D4 recognizes a common extracellular epitope on MICA and MICB glycoproteins, transmembrane ligands of NKG2D, and is able to block NKG2D-mediated activation of NK cells and cytotoxic T cells.
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