NKG2A-CD94 Heterodimer Protein, Human (HEK293, mFc)

NKG2A Protein, a crucial immune inhibitory receptor, forms a complex with KLRD1 on lymphocyte subsets for self-nonself discrimination. Recognizing HLA-E loaded with self-peptides, it monitors MHC class I expression in healthy cells, promoting self-tolerance. NKG2A transmits signals through ITIMs, recruiting tyrosine phosphatases to counteractivate receptors. As a key inhibitor on NK cells, it regulates their functions, distinguishing harmless from pathogenic antigens. In the tumor microenvironment, NKG2A acts as an immune inhibitory checkpoint, contributing to cell exhaustion. During viral infection, it inhibits NK cell cytotoxicity, facilitating viral immune escape. NKG2A-CD94 Heterodimer Protein, Human (HEK293, mFc) is a recombinant protein dimer complex containing human-derived NKG2A-CD94 Heterodimer protein, expressed by HEK293, with C-mFc labeled tag. NKG2A-CD94 Heterodimer Protein, Human (HEK293, mFc), has molecular weight of 70-90 kDa.

NKG2A Protein, an immune inhibitory receptor crucial for self-nonself discrimination, forms a complex with KLRD1 on cytotoxic and regulatory lymphocyte subsets, recognizing the non-classical major histocompatibility (MHC) class Ib molecule HLA-E loaded with self-peptides from the signal sequence of classical MHC class Ia molecules. This recognition allows cytotoxic cells to monitor MHC class I expression in healthy cells and promotes self-tolerance. Upon binding to HLA-E-peptide complexes, NKG2A transmits intracellular signals through two immunoreceptor tyrosine-based inhibition motifs (ITIMs), recruiting INPP5D/SHP-1 and INPPL1/SHP-2 tyrosine phosphatases to oppose signals from activating receptors. As a key inhibitory receptor on natural killer (NK) cells, NKG2A regulates their activation and effector functions, countering T cell receptor signaling on a subset of memory/effector CD8-positive T cells and distinguishing harmless from pathogenic antigens. In the HLA-E-rich tumor microenvironment, NKG2A acts as an immune inhibitory checkpoint, contributing to the progressive loss of effector functions in NK cells and tumor-specific T cells, a phenomenon known as cell exhaustion. Notably, during viral infection, NKG2A recognizes HLA-E in complex with human cytomegalovirus-derived peptides, inhibiting NK cell cytotoxicity and facilitating viral immune escape.

Human

HEK293

C-mFc

P26715 (R100-L233)&Q13241 (S34-I179)

3821  [NCBI]&3824  [NCBI]

70-90 kDa

Greater than 95% as determined by Tris-Bis PAGE.

<1 EU/μg, determined by LAL method.