Flow cytometric analysis of human PBMC (human peripheral blood mononuclear cells) labelling Mouse Anti-Human CD314 antibody at 1/200 dilution (1 μg) / (right panel) compared with a Mouse IgG1 Isotype Control / (left panel). Goat Anti-Mouse IgG Alexa Fluor® 488 was used as the secondary antibody. Then cells were stained with CD3 - Brilliant Violet 421™ antibody separately. Flow cytometry and data analysis were performed using Agilent NovoCyte Quanteon and FlowJo™ software.
Product Details
Product Details
Product Specification
| Host | Mouse |
| Antigen | CD314 (NKG2D) |
| Synonyms | NKG2-D type II integral membrane protein; Killer cell lectin-like receptor subfamily K member 1; NK cell receptor D; NKG2-D-activating NK receptor; D12S2489E; KLRK1 |
| Location | Cell membrane |
| Accession | P26718 |
| Clone Number | S-4154 |
| Antibody Type | Mouse mAb |
| Isotype | IgG1,k |
| Application | FCM |
| Reactivity | Hu |
| Positive Sample | Human PBMC |
| Purification | Protein G |
| Concentration | 2 mg/ml |
| Conjugation | Unconjugated |
| Physical Appearance | Liquid |
| Storage Buffer | PBS pH7.4 |
| Stability & Storage | 12 months from date of receipt / reconstitution, 2 to 8 °C as supplied |
Dilution
| application | dilution | species |
| FCM | 1:200 | Hu |
Background
CD314, also known as NKG2D (Natural Killer Group 2D), is a type II transmembrane glycoprotein and a member of the C-type lectin-like receptor family that serves as an activating receptor expressed on the surface of natural killer (NK) cells, CD8+ T cells, γδ T cells, and NKT cells. It functions as a homodimeric receptor that recognizes stress-induced ligands, including MICA, MICB, and ULBP1-6 (UL16-binding proteins) in humans, which are upregulated on infected, transformed, or damaged cells due to cellular stress, DNA damage, or viral infection. Upon ligand engagement, NKG2D associates with the adaptor protein DAP10 (DNAX-activating protein of 10 kDa) through a charged transmembrane interaction, triggering phosphoinositide 3-kinase (PI3K)-dependent signaling pathways that promote cytotoxicity, cytokine production, and enhanced immune surveillance. Unlike many other NK cell receptors, NKG2D signaling is not inhibited by self-MHC class I molecules, making it a critical mechanism for distinguishing healthy cells from aberrant cells in the context of cancer immunosurveillance, viral defense, and autoimmune regulation. Dysregulation of the NKG2D-ligand axis has been implicated in various pathological conditions, including tumor immune evasion through ligand shedding or downregulation, as well as autoimmune diseases such as rheumatoid arthritis and type 1 diabetes, highlighting its significance as a therapeutic target in immuno-oncology and immunotherapy development.
Picture
Picture
FC
