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Description
Invivo anti-Mouse CD314 (NKG2D) Recombinant mAbProduct Specification Host Rat 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; Nkg2d; Klrk1 Location Cell membrane Accession O54709 Clone Number S R664 Antibody Type Rat mAb Isotype Rat IgG1,k Application FCM, in vivo CD314 blockade, in vitro CD314 blockade Reactivity Ms Positive Sample C57BL 6 mouse splenocytes
Product Specification
| Host | Rat |
| 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; Nkg2d; Klrk1 |
| Location | Cell membrane |
| Accession | O54709 |
| Clone Number | S-R664 |
| Antibody Type | Rat mAb |
| Isotype | Rat IgG1,k |
| Application | FCM, in vivo CD314 blockade, in vitro CD314 blockade |
| Reactivity | Ms |
| Positive Sample | C57BL/6 mouse splenocytes |
| Purification | Protein G |
| Concentration | 5 mg/ml |
| Purity | >95%(Determined by SDS-PAGE) |
| Endotoxin | <1EU/mg |
| Conjugation | Unconjugated |
| Physical Appearance | Liquid |
| Storage Buffer | PBS pH7.4, containing no preservative |
| Stability & Storage | 2 to 8 °C for 2 weeks under sterile conditions; |
Dilution
| application | dilution | species |
| FCM | 1:500 | Ms |
Background
NKG2D is a type II transmembrane C-type lectin-like receptor expressed as a disulfide-linked homodimer on virtually all human and mouse NK cells, γδ T cells, and CD8+ αβ T cells; upon engagement by stress-inducible MHC class I–related ligands (MICA/B, ULBPs in humans; Rae-1, H60, Mult1 in mice) it couples to the DAP10 (and in mouse also DAP12) adaptor to deliver phosphotyrosine signals that powerfully lower activation thresholds, costimulate cytotoxicity, and drive proliferation and cytokine release, thereby forming a central surveillance axis that eliminates transformed, infected, or otherwise stressed cells but also contributes to immune-mediated pathologies when ligand expression becomes chronic.
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