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Recombinant Human MIC-B produced in E.coli is a protein with 326 amino acid residues containing the extracellular domain of mature human MICB (amino acid residues Ala23 – Tyr312) and having a molecular mass of approximately 37 kDa.
Measured by its ability to bind MICB antibody in a ELISA.
Less than 1EU/μg of rHuMIC-B as determined by LAL method.
>95% by SDS-PAGE and HPLC analyses.
This lyophilized preparation is stable at 2-8°C, but should be kept at -20°C for long term storage, preferably desiccated. Upon reconstitution, the preparation is stable for up to one week at 2-8°C. For maximal stability, apportion the reconstituted preparation into working alire 0t -C to -70°C. Avoid repeated freeze/thaw cycles.
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Reconstitute in sterile distilled water or aqueous buffer containing 0.1% BSA to a concentration of 0.1-1.0 mg/mL. Stock solutions should be apportioned into working aliquots and stored at <-20°C. Further dilutions should be made in appropriate buffered solutions.
MIC-B (MHC class I chain-related gene B) is a transmembrane glycoprotein that functions as a ligand for human NKG2D. A closely related protein, MIC-A, shares 85% amino acid identity with MIC-B. These 2 proteins are distantly related to the MHC class I proteins. MIC-A and MIC-B (MIC-A/B) possess three extracellular immunoglobulin-like domains, but have no capacity to bind peptide or interact with β2-microglobulin. The genes encoding MIC-A/B are found within the major histocompatibility complex on human chromosome 6. The MIC-B locus is polymorphic with more than 15 recognized human alleles. MIC-A/B are minimally expressed on normal cells, but are frequently expressed on epithelial tumors and can be induced by bacterial and viral infections.MIC-A/B are ligands for NKG2D, an activating receptor expressed on NK cells, NKT cells, γδ T cells, and CD8+ αβ T cells. Recognition of MIC-A/B by NKG2D results in the activation of cytolytic activity and/or cytokine production by these effector cells. MIC-A/B recognition is involved in tumor surveillance, viral infections, and autoimmune diseases. The release of soluble forms of MIC-A/B from tumors down-regulates NKG2D surface expression on effector cells resulting in the impairment of anti-tumor immune response.
MHC class I receptor activity;molecular_function;protein binding.
AS; HLAB; HLAC; SPDA1; HLA-B73; HLA-B-7301; major histocompatibility complex, class I, B; ankylosing spondylitis; 1B53_HUMAN; HLA class I histocompatibility antigen, B-53; alpha chain [Precursor]; MHC class I antigen; B*53; Bw-53; HLAB;B'DT;B-12;B-21;B-5;HLA-B-5501;OTTHUMP00000034826; HLA class I histocompatibility antigen, B alpha chain; HLA class I histocompatibility antigen, B alpha chain precursor; Human transforming growth factor-beta induced gene product (BIGH3);mRNA, complete cds; MHC HLA-B cell surface glycoprotein;MHC class I HLA-B40MD alpha chain; MHC class I HLA-C antigen; MHC class I antigen B*13; MHC class I antigen HLA-B heavy chain; MHC class I antigen SHCHA; ankylosing spondylitis; leucocyte antigen C; leukocyte antigen class I-B; lymphocyte antigen; major histocompatibility complex class I B; major histocompatibility complex, class I, B.