NKG2D/CD314 Protein, Mouse (HEK293, Fc)

NKG2D/CD314 Protein functions as an activating and costimulatory receptor critical for immunosurveillance, binding to stress-inducible ligands on autologous tumor cells and virus-infected cells. This engagement triggers stimulatory and costimulatory innate immune responses in activated killer (NK) cells, leading to cytotoxic activity. In CD8(+) T-cell-mediated adaptive immune responses, NKG2D acts as a costimulatory receptor for the T-cell receptor (TCR), amplifying T-cell activation and stimulating perforin-mediated elimination of ligand-expressing tumor cells. Signaling involves calcium influx, culminating in TNF-alpha expression. NKG2D participates in NK cell-mediated bone marrow graft rejection and may regulate NK cell differentiation and survival. The protein forms a homodimer through disulfide linkage and a heterohexamer with HCST/DAP10, crucial for NK cell surface expression and induction of cytotoxicity. It interacts with various ligands, including RAET1A, RAET1B, RAET1C, RAET1D, RAET1E, H60, and MULT1, belonging to MHC class I-related glycoproteins subfamilies. Additionally, NKG2D interacts with CEACAM1, recruiting PTPN6 for VAV1 dephosphorylation, highlighting its role in orchestrating complex immune responses.