PE/Cyanine7 anti-human CD158e1 KIR3DL1, NKB1 Antibody anti-CD158e1 - DX9,BioLegend,312720

The DX9 antibody reacts with the KIR (killer cell inhibitory receptor) designated NKB1 or KIR3DL1. Additional reported applications (for the relevant formats) include: immunoprecipitation1and restoring the NK cell cytotoxicity4,8. The LEAF™ purified antibody (Endotoxin <0.1 EU/µg, Azide-Free, 0.2 µm filtered) is recommended for functional assays (Cat. No. 312710).

Host

Mouse

Reactivity

Human

Application

FC - Quality tested

Platform ID

BAB095743430

BioLegend

Headquarters

8999 BioLegend Way San Diego, CA 92121 United States

Contact

Tel: 1-858-455-9588
Fax: +49 (4131) 7023913

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Product Specifications
Scientific Background

Specifications

NamePE/Cyanine7 anti-human CD158e1 KIR3DL1, NKB1 Antibody anti-CD158e1 - DX9
Cat. No.312720
HostMouse
RRIDAB_2563363 (BioLegend Cat. No. 312719)AB_2563364 (BioLegend Cat. No. 312720)
IsotypeMouse IgG1, κ
ReactivityHuman
ApplicationFC - Quality tested
ClonalityMonoclonal
Clone NumberDX9
ConcentrationLot-specific (to obtain lot-specific concentration and expiration, please enter the lot number in ourCertificate of Analysisonline tool.)
TargetCD158e1
ImmunogenHuman NK cell clone VL186-1.6
PurityThe antibody was purified by affinity chromatography and conjugated with PE/Cyanine7 under optimal conditions.
FormulationPhosphate-buffered solution, pH 7.2, containing 0.09% sodium azide and BSA (origin USA)
StorageThe antibody solution should be stored undiluted between 2°C and 8°C, and protected from prolonged exposure to light.Do not freeze.
Regulatory StatusResearch Use Only

Scientific Background

CD158e1, also known as NKB1, is a 70 kD member of the immunoglobulin superfamily that is expressed on a subset of natural killer cells and T cells at varying levels among individuals. NKB1 is a type I membrane protein containing two immunoglobulin C2-type domains. The interaction of NKB1 with specific HLA-B antigens on a target cell (the HLA-Bw4 allele, for example) inhibits cytotoxicity and prevents target cell lysis and death. The interactions between KIR and MHC class I are thought to be important in NK and T cell regulation following antigen stimulation. The absence of ligands for KIRs may lower the threshold for activation through activating receptors and increase inflammation and susceptibility to autoimmune disease.

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