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Description
Biotin Mouse Anti-Human CD314 (NKG2D) Antibody (S-4154)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 0. 2 mg ml Conjugation Biotin
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 | 0.2 mg/ml |
| Conjugation | Biotin |
| Physical Appearance | Liquid |
| Storage Buffer | PBS pH7.4, 0.03% Proclin 300 |
| Stability & Storage | 12 months from date of receipt / reconstitution, 2 to 8 °C as supplied |
Dilution
| application | dilution | species |
| FCM | 5μl per million cells in 100μl volume | 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.
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