MIC-A (MHC class I chain-related gene A) is a single-pass type I member protein. It is expressed on the cell surface in gastric epithelium, endothelial cells and fibroblasts and in the cytoplasm in keratinocytes and monocytes. Additionally, MIC-A can be induced by bacterial and viral infections. It shares 85 % amino acid identity with MIC-B and they are distantly related to the MHC class I proteins. Because they possess three extracellular Ig-like domains, but unlike classical MHC class I molecules. They do not form a heterodimer with beta2 microglobulin, but bind as a monomer to a KLRK1/NKG2D that is an activating receptor expressed on NK cells, NKT cells, gammadelta T cells, and CD8+ alphabeta T cells. Recognition of MICA by NKG2D results in the activation of cytolytic activity and/or cytokine production by these effector cells. MIC-A recognition plays an important role in tumor surveillance, viral infections, and autoimmune diseases.
Source
Molecular Weight
Biological Activity
Fully biologically active when compared to standard. The specific activity is determined by binding MICA antibody in ELISA.
Appearance
Sterile Filtered White lyophilized (freeze-dried) powder.
Formulation
Lyophilized from a 0.2 um filtered concentrated solution in PBS, pH 7.4, and 8 M Urea.
Endotoxin
Less than 1 EU/ug of rHuMIC-A, His as determined by LAL method.
Reconstitution
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Reconstitute in sterile distilled water to a concentration of 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, which contain 8 M Urea.
Stability and Storage
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.- 3 months, -20 to -70 °C under sterile conditions after reconstitution.
References
1. Yao Z, Volgger A, Helmberg W, et al. 1999. Eur J Immunogenet, 26: 225-32.2. Li P, Willie ST, Bauer S, et al. 1999. Immunity, 10: 577-84.3. Petersdorf EW, Shuler KB, Longton GM, et al. 1999. Immunogenetics, 49: 605-12.4. Komatsu-Wakui M, Tokunaga K, Ishikawa Y, et al. 1999. Immunogenetics, 49: 620-8.5. Gambelunghe G, Ghaderi M, Cosentino A, et al. 2000. Diabetologia, 43: 507-14.
