Human NKG2-A/NKG2-B Type II Integral Membrane Protein (KLRC1) Protein
234€ (1 µg)
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935106861
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name
Human NKG2-A/NKG2-B Type II Integral Membrane Protein (KLRC1) Protein
category
Proteins and Peptides
provider
Abbexa
reference
abx680119
tested applications
SDS-PAGE
Description
Human NKG2-A/NKG2-B Type II Integral Membrane Protein (KLRC1) Protein is a recombinant protein produced in Sf9, Baculovirus cells.
Documents del producto
Instrucciones
Data sheet
Product specifications
| Category | Proteins and Peptides |
| Immunogen Target | NKG2-A/NKG2-B Type II Integral Membrane Protein (KLRC1) |
| Host | Insect |
| Origin | Human |
| Conjugation | Unconjugated |
| Expression | Recombinant |
| Purity | > 90% (SDS-PAGE) |
| Size 1 | 1 µg |
| Size 2 | 5 µg |
| Size 3 | 50 µg |
| Form | Liquid |
| Tested Applications | SDS-PAGE |
| Availability | Shipped within 5-10 working days. |
| Dry Ice | No |
| Alias | NKG2,NKG2A,CD159A,NKG2-A/NKG2-B type II integral membrane protein,CD159 antigen-like family member A,NK cell receptor A,NKG2-A/B-activating NK receptor |
| Background | Protein KLRC1 |
| Status | RUO |
| Note | This product is for research use only. Not for human consumption, cosmetic, therapeutic or diagnostic use. |
Descripción
Killer Cell Lectin-Like Receptor C1 (KLRC1), also known as NKG2A, is a member of the natural killer (NK) cell receptor family and is primarily expressed on NK cells and certain T cell subsets. KLRC1 forms a heterodimer with CD94, and this complex specifically binds to HLA-E, a non-classical major histocompatibility complex (MHC) class I molecule. Upon ligand binding, KLRC1 transmits inhibitory signals through its immunoreceptor tyrosine-based inhibition motif (ITIM), suppressing the activation of NK cells and preventing cytotoxicity. This mechanism is crucial for maintaining immune tolerance and preventing autoimmunity. KLRC1 expression and activity are finely regulated during immune responses, with higher expression levels often associated with a suppressive immune environment. Research has shown that tumor cells and some pathogens exploit KLRC1-mediated inhibition to evade immune surveillance, making it a target of interest for immunotherapeutic strategies. By blocking KLRC1 signaling, immune activation can be enhanced, potentially improving responses against cancers and chronic infections. Additionally, polymorphisms in the KLRC1 gene have been linked to variations in susceptibility to autoimmune diseases and certain infections, underscoring its significance in immunoregulation and disease pathogenesis.
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