Human Interleukin 13 Receptor, Alpha 1, IL13RA1 ELISA Kit

Name: Human Interleukin 13 Receptor, Alpha 1, IL13RA1 ELISA Kit
SKU: DEIA258
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

Plasma, tissue homogenates and other biological fluids.

Species Reactivity

Human

Detection Method

sELISA

Intended Use

The human IL13RA1 / CD213a1 ELISA Pair Set is for the quantitative determinationof human IL13RA1.
This ELISA Pair Set contains the basic components required for the development of sandwich ELISAs.

Contents of Kit

Capture Antibody: 0.5 mg/mL of mouse anti-IL13RA1 monoclonal antibody. Dilute to a working concentration of 2.0 μg/mL in CBS before coating.
Detection Antibody: 0.5 mg/mL of mouse anti-IL13RA1 monoclonal antibody conjugated to horseradish-peroxidase (HRP). Dilute to working concentration of 1.0 μg/mL in detection antibody dilution buffer before use.dish-peroxidase (HRP) (in PBS, 50 % HRP-Protector, pH 7.4, store at 4°C). Dilute to working concentration of 0.5 μg/mL in detection antibody dilution buffer before use.
Standard: Each vial contains 80 ng of recombinant IL13RA1. Reconstitute with 1 mL detection antibody dilution buffer. After reconstitution, store at -20°C to -80°C in a manual defrost freezer. A six-point standard curve usi ng 2-fold serial dilutions in sample dilution buffer, and a high standard of 2000 pg/mL is recommended.

Storage

Capture Antibody: Aliquot and store at -20°C to -80°C for up to 6 months from date of receipt. Avoid repeated freeze-thaw cycles.
Detection Antibody: Store at 4°C and protect it from prolonged exposure to light for up to 6 months from date of receipt. Do not freeze!
Standard: Store lyophilized standard at -20°C to -80°C for up to 6 months from date of receipt. Aliquot and store the reconstituted standard at -80°C for up to 1 month. Avoid repeated freezethaw cycles.

Sensitivity

The minimum detectable dose of Human IL13RA1 / CD213a1 was determined to be approximately 31.25 pg/ml.
This is defined as at least three times standard deviations above the mean optical density of 10 replicates of the zero standard.

General Description

Interleukin 13 receptor, alpha 1, also known as IL13RA1/IL-13RA1 and CD213A1 (cluster of differentiation 213A1), is a subunit of the interleukin 13 receptor. This subunit forms a receptor complex with IL4 receptor alpha, a subunit shared by IL13 and IL4 receptors. IL13RA1/IL-13RA1 serves as a primary IL13-binding subunit of the IL13 receptor, and may also be a component of IL4 receptors. This protein has been shown to bind tyrosine kinase TYK2, and thus may mediate the signaling processes that lead to the activation of JAK1, STAT3 and STAT6 induced by IL13 and IL4. IL13RA1/IL-13RA1 binds with low affinity to interleukin-13 (IL13). This subunit together with IL4RA can form a functional receptor for IL13. IL13RA1/IL-13RA1 also serves as an alternate accessory protein to the common cytokine receptor gamma chain for interleukin-4 (IL4) signaling, but cannot replace the function of IL2RG in allowing enhanced interleukin-2 (IL2) binding activity.

Standard Curve

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Documents

pdf COA

pdf SDS

pdf Datasheet

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Customer Reviews

References

A protective role for IL-13 receptor alpha 1 in bleomycin-induced pulmonary injury and repair

MUCOSAL IMMUNOLOGY

Authors: Karo-Atar, D.; Bordowitz, A.; Wand, O.; Pasmanik-Chor, M.; Fernandez, I. E.; Itan, M.; Frenkel, R.; Herbert, D. R.; Finkelman, F. D.; Eickelberg, O.; Munitz, A.

Abstract

Molecular mechanisms that regulate lung repair vs. progressive scarring in pulmonary fibrosis remain elusive. Interleukin (IL)-4 and IL-13 are pro-fibrotic cytokines that share common receptor chains including IL-13 receptor (R) alpha 1 and are key pharmacological targets in fibrotic diseases. However, the roles of IL-13R alpha 1 in mediating lung injury/repair are unclear. We report dysregulated levels of IL-13 receptors in the lungs of bleomycin-treated mice and to some extent in idiopathic pulmonary fibrosis patients. Transcriptional profiling demonstrated an epithelial cell-associated gene signature that was homeostatically dependent on IL-13R alpha 1 expression. IL-13R alpha 1 regulated a striking array of genes in the lung following bleomycin administration and Il13ra1 deficiency resulted in exacerbated bleomycin-induced disease. Increased pathology in bleomycin-treated Il13ra1(-/-) mice was due to IL-13R alpha 1 expression in structural and hematopoietic cells but not due to increased responsiveness to IL-17, IL-4, IL-13, increased IL-13R alpha 2 or type 1 IL-4R signaling. These data highlight underappreciated protective roles for IL-13R alpha 1 in lung injury and homeostasis.

Modulation of Transcriptional and Inflammatory Responses in Murine Macrophages by the Mycobacterium tuberculosis Mammalian Cell Entry (Mce) 1 Complex

PLOS ONE

Authors: Stavrum, Ruth; Stavrum, Anne-Kristin; Valvatne, Havard; Riley, Lee W.; Ulvestad, Elling; Jonassen, Inge; Assmus, Joerg; Doherty, T. Mark; Grewal, Harleen M. S.

Abstract

The outcome of many infections depends on the initial interactions between agent and host. Aiming at elucidating the effect of the M. tuberculosis Mce1 protein complex on host transcriptional and immunological responses to infection with M. tuberculosis, RNA from murine macrophages at 15, 30, 60 min, 4 and 10 hrs post-infection with M. tuberculosis H37Rv or Delta-mce1 H37Rv was analyzed by whole-genome microarrays and RT-QPCR. Immunological responses were measured using a 23-plex cytokine assay. Compared to uninfected controls, 524 versus 64 genes were up-regulated by 15 min post H37Rv- and Delta-mce1 H37Rv-infection, respectively. By 15 min post-H37Rv infection, a decline of 17 cytokines combined with up-regulation of Ccl24 (26.5-fold), Clec4a2 (23.2-fold) and Pparc (10.5-fold) indicated an anti-inflammatory response initiated by IL-13. Down-regulation of Il13ra1 combined with up-regulation of Il12b (30.2-fold), suggested switch to a pro-inflammatory response by 4 hrs post H37Rv-infection. Whereas no significant change in cytokine concentration or transcription was observed during the first hour post Delta-mce1 H37Rv-infection, a significant decline of IL-1b, IL-9, IL-13, Eotaxin and GM-CSF combined with increased transcription of Il12b (25.1-fold) and Inb1 (17.9-fold) by 4 hrs, indicated a pro-inflammatory response. The balance between pro-and anti-inflammatory responses during the early stages of infection may have significant bearing on outcome.