Ultra-LEAF™ Purified anti-mouse IL-13Rα2 (BA) Antibody, IL-13Rα2, W19369C,BioLegend,947903

Host

Rat

Reactivity

Mouse

Application

Neut - Quality tested

Platform ID

BAB959064010

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

NameUltra-LEAF™ Purified anti-mouse IL-13Rα2 (BA) Antibody, IL-13Rα2, W19369C
Cat. No.947903
HostRat
RRIDAB_2922648 (BioLegend Cat. No. 947903)AB_2922648 (BioLegend Cat. No. 947904)
IsotypeRat IgG1, κ
ReactivityMouse
ApplicationNeut - Quality tested
ClonalityMonoclonal
Clone NumberW19369C
ConcentrationThe antibody is bottled at the concentration indicated on the vial, typically between 2 mg/mL and 3 mg/mL. To obtain lot-specific concentration and expiration, please enter the lot number in ourCertificate of Analysisonline tool.
TargetIL-13Ralpha2
ImmunogenRecombinant mouse IL-13Rα2-Fc chimera
PurityThe Ultra-LEAF™ (Low Endotoxin, Azide-Free) antibody was purified by affinity chromatography.
Formulation0.2 µm filtered in phosphate-buffered solution, pH 7.2, containing no preservative.
StorageThe antibody solution should be stored undiluted between 2°C and 8°C. This Ultra-LEAF™ solution contains no preservative; handle under aseptic conditions.
Regulatory StatusResearch Use Only

Scientific Background

IL-13 is a key mediator in the pathogenesis of allergic inflammation. Its receptor is comprised of IL-4Rα and IL-13Rα1, which transduct the signaling to the downstream STAT6 pathway. IL-13Rα2, also known as IL-13Ra2 and IL-13BP, serves as a decoy receptor to attenuate IL-13-induced response. IL-13Rα2 binds IL-13 with 100-300 folds higher affinity than does IL-13Rα1, but IL-13Rα2 lacks signaling motifs on its cytoplasmic tail. Mice deficient in IL-13Rα2 showed increased IgE level and IFNγ production, consistent with a phenotype of enhanced IL-13 effects. Airway hyperresponsiveness and inflammation was enhanced in IL-13Rα2 transgene mice, indicating that IL-13Rα2 blocks IL-13 mediated response. In mice, there are two discrete transcripts generated by alternative splicing, producing membrane-bound and secreted forms, respectively. Some evidences indicated that MMP-8 contributes to soluble forms of IL-13Rα2 by cleaving membrane-bound IL-13Rα2. In human, only membrane-bound transcript was found and soluble forms were absent in human plasma.

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