PE anti-human CD158b/j KIR2DL2/L3/S2 Antibody anti-CD158b/j - DX27,BioLegend,312605

The DX27 monoclonal antibody reacts with a common epitope of KIR2DL2 (CD158b1, p58.2), KIR2DL3 (CD158b2, p58.3), and KIR2DS2 (CD158j, p50.2). Additional reported applications (for the relevant formats) include: restoring the NK cell cytotoxicity1,5.This clone has been tested in-house and determined to not be suitable for applications in immunohistochemistry of paraffin-embedded tissue sections (IHC-P).

Host

Mouse

Reactivity

Human

Application

FC - Quality tested

Platform ID

BAB095443574

BioLegend

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Contact

Tel: 1-858-455-9588
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Product Specifications
Scientific Background

Specifications

NamePE anti-human CD158b/j KIR2DL2/L3/S2 Antibody anti-CD158b/j - DX27
Cat. No.312605
HostMouse
RRIDAB_2296485 (BioLegend Cat. No. 312605)AB_2130554 (BioLegend Cat. No. 312606)
IsotypeMouse IgG2a, κ
ReactivityHuman
ApplicationFC - Quality tested
ClonalityMonoclonal
Clone NumberDX27
ConcentrationLot-specific (to obtain lot-specific concentration and expiration, please enter the lot number in ourCertificate of Analysisonline tool.)
TargetCD158b/j
PurityThe antibody was purified by affinity chromatography, and conjugated with PE 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

CD158b is expressed on natural killer cells and a subset of T cells. It is a member of the immunoglobulin superfamily containing two immunoglobulin C2-type domains. Both variants and alternative isoforms of CD158b have been reported. The interaction of CD158b with specific HLA-C antigens on a target cell (HLA-Cw1, HLA-Cw3, HLA-Cw7 alleles, 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 cell 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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