Lane 1: U937
Lane 2: Mouse bone marrow
Rabbit polyclonal primary
MICA + MICB Rabbit Polyclonal Antibody (ER1803-95)
Recombinant protein within human mica + micb aa 182-325 / 383.
U937, Mouse bone marrow, A431, rat skin tissue, human lung cancer tissue, human colon tissue, human breast carcinoma tissue, mouse stomach tissue.
Store at +4C after thawing. Aliquot store at -20C. Avoid repeated freeze / thaw cycles.
1*PBS (pH7.4), 0.2% BSA, 50% Glycerol. Preservative: 0.05% Sodium Azide.
Protein affinity purified.
MICA + MICB
MHC class I chain-related protein A antibody; MHC class I chain-related protein B antibody; MHC class I polypeptide related sequence A antibody; MHC class I polypeptide related sequence B antibody; MHC class I polypeptide-related sequence A antibody; MIC-A antibody; micA antibody; MICA_HUMAN antibody; MICB antibody
Belongs to the MHC class I family. MIC subfamily.
Widely expressed with the exception of the central nervous system where it is absent. Expressed in many, but not all, epithelial tumors of lung, breast, kidney, ovary, prostate and colon. In hepatocellular carcinomas, expressed in tumor cells but not in surrounding non-cancerous tissue.
Proteolytically cleaved and released from the cell surface of tumor cells.
Cell membrane. Cytoplasm.
MHC class I polypeptide-related sequence A/B (MICA/B) is a cell surface glycoprotein encoded by the MICA/B gene located within MHC locus. MICA and MICB are related to MHC class I and has similar domain structure, which is made up of external α1α2α3 domain, transmembrane segment and C-terminal cytoplasmic tail. MICA/B rather functions as a stress-induced ligand for NKG2D receptor. MICA is broadly recognized by NK cells, γδ T cells, and CD8+ αβ T cells which carry NKG2D receptor on their cell surface. As a result of NKG2D-MICA engagement, effector cytolytic responses of T cells and NK cells against epithelial tumor cells expressing MICA are initiated. MICA/B are not associated with β2-microglobulin nor binds peptides as conventional MHC class I molecules do. The heat shock stress pathway is involved in the regulation of MICA expression as transcription of MICA is regulated by promoter heat shock element.