More info
Assay Range | 62.5--4000 pg/mL |
Sensitivity | 10.0 pg/mL |
Size | 96T |
Storage | Store at 2 - 8ºC. Keep reconstituted standard and detection Ab at -20 ºC |
Assay Principle | Sandwich ELISA |
Sample volume | 100 µL final volume, dilution factor varies on samples |
Detection Method | Chromogenic |
Kit Components
1. Recombinant Human MICB standard: 2 vials
2. One 96-well plate precoated with anti- Human MICB Ab
3. Sample diluent buffer: 12 mL - 1
4. Detection antibody: 130 µL, dilution 1:100
5. Streptavidin-HRP: 130 µL, dilution 1:100
6. Antibody diluent buffer: 12 mL x1
7. Streptavidin-HRP diluent buffer: 12 mL x1
8. TMB developing agent: 10 mL x1
9. Stop solution: 10 mL x1.
10. Washing solution (20x): 25 mL x1.
Background
MICB (MHC class I chain related gene B) is a transmembrane glycoprotein encoded by the MICB gene in humans. Structurally and functionally, MICB is closely related to the protein MICA. They share 85% amino acid (aa) identity and possess three extracellular immunoglobulin-like domains. MICB is structurally similar to MHC class I molecules but has no capacity to bind peptide or interact with β2-microglobulin. MICB is minimally expressed on normal cells, but are frequently expressed on epithelial tumors and can be induced by bacterial and viral infections. Expression of MICB is also induced by various stimuli, such as heat shock, oxidative stress, retinoic acid, IFN-alpha and the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine. MICB is a ligand for KLRK1/NKG2D, an activating receptor expressed on NK cells, NKT cells, γδ T cells, and CD8+ αβ T cells. KLRK1 forms a complex with HCST/DAP10 in which KLRK1 binds MICB while HCST acts as an adapter molecule to activate the downstream signal transduction. Interaction of MICB/ KLRK1 initiates the activation of cytolytic activity and/or cytokine production by these effector cells. MICB signaling is involved in tumor surveillance, viral infections, and autoimmune diseases. It is reported that the release of soluble form of MICB from tumors down-regulates KLRK1 surface expression on effector cells and thus impairs antitumor immune response.