MICB Antibody – Mouse Monoclonal

This gene encodes a heavily glycosylated protein which is a ligand for the NKG2D type II receptor. Binding of the ligand activates the cytolytic response of natural killer (NK) cells, CD8 alphabeta T cells, and gammadelta T cells which express the receptor. This protein is stress-induced and is similar to MHC class I molecules; however, it does not associate with beta-2-microglobulin or bind peptides. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jan 2014]

MICB: Seems to have no role in antigen presentation. Acts as a stress-induced self-antigen that is recognized by gamma delta T cells. Ligand for the KLRK1/NKG2D receptor. Binding to KLRK1 leads to cell lysis. Genetic variations in MICA are a cause of susceptibility to rheumatoid arthritis (RA). It is a systemic inflammatory disease with autoimmune features and a complex genetic component. It primarily affects the joints and is characterized by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. The MICB*004 allele is associated with rheumatoid arthritis. Genetic variation in MICB is associated with cytomegalovirus and herpes simplex virus I seropositivity and this may be associated with schizophrenia risk. Belongs to the MHC class I family. MIC subfamily. 3 isoforms of the human protein are produced by alternative splicing.

Protein type: Membrane protein, integral

Chromosomal Location of Human Ortholog: 6p21.3

Cellular Component: cell surface; integral to membrane; plasma membrane

Molecular Function: beta-2-microglobulin binding; antigen binding; natural killer cell lectin-like receptor binding

Biological Process: antigen processing and presentation; regulation of immune response; response to retinoic acid; viral reproduction; natural killer cell mediated cytotoxicity; response to heat; cytolysis; immune response-activating cell surface receptor signaling pathway; response to oxidative stress; negative regulation of defense response to virus by host; gamma-delta T cell activation; T cell mediated cytotoxicity