Human Interleukin 13 Receptor, Alpha 1, IL13RA1 ELISA Kit

Name: Human Interleukin 13 Receptor, Alpha 1, IL13RA1 ELISA Kit
SKU: CKERS-IL13RA1-255H
Rating: 5 (1 reviews)

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

COA

SDS

Datasheet

Summary

Species Reactivity

Human

Detection Method

Sandwich ELISA

Intended Use

The human IL13RA1 ELISA kit is for the quantitative determination of human IL13RA1.
This ELISA kit contains the basic components required for the development of sandwich ELISAs. Each kit contains sufficient materials to run ELISAs on five 96-well plates.

Contents of Kit

1. Bring all reagents to room temperature before use.
2. Capture Antibody: 0.5 mg/mL of mouse anti-IL13RA1 monoclonal antibody.
3. Detection Antibody: 0.5 mg/mL of #rabbit anti-IL13RA1 monoclonal antibody conjugated to horseradish-peroxidase(HRP). Dilute to a working concentration of 1.0 μg/mL in detection antibody dilution buffer before use.
4. Standard: Each vial contains 80 ng of recombinant IL13RA1. Reconstitute with 1 mL detection antibody dilution buffer. After reconstitution, store at -20°C to -70°C in a manual defrost freezer. A seven-point standard curve using 2-fold serial dilutions in sample dilution buffer, and a high standard of 2,000 pg/mL is recommended.

Storage

Detection Antibody should be protected from prolonged exposure to light. Aliquot all other reagents and store at -20°C to -70°C in a manual defrost freezer.

Sensitivity

The minimum detectable dose of human IL13RA1 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.

Citations

Have you cited CKERS-IL13RA1-255H in a publication? Let us know and earn a reward for your research.

Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

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.

Polymorphisms in IL13 pathway genes in asthma and chronic obstructive pulmonary disease

ALLERGY

Authors: Beghe, B.; Hall, I. P.; Parker, S. G.; Moffatt, M. F.; Wardlaw, A.; Connolly, M. J.; Fabbri, L. M.; Ruse, C.; Sayers, I.

Abstract

P>Background: Asthma and chronic obstructive pulmonary disease (COPD) are chronic respiratory diseases involving an interaction between genetic and environmental factors. Interleukin-13 (IL13) has been suggested to have a role in both asthma and COPD. We investigated whether single nucleotide polymorphisms (SNPs) in the IL13 pathway may contribute to the susceptibility and severity of asthma and COPD in adults. Methods: Twelve SNPs in IL13 pathway genes -IL4, IL13, IL4RA, IL13RA1, IL13RA2 and STAT6- were genotyped in subjects with asthma (n = 299) and in subjects with COPD or healthy smokers (n = 992). Genetic association was evaluated using genotype and allele models for asthma severity, atopy phenotypes and COPD susceptibility. Linear regression was used to determine the effects of polymorphism on baseline lung function (FEV(1), FEV(1)/FVC). Results: In asthmatics, three IL13 SNPs - rs1881457(-1512), rs1800925(-1111) and rs20541(R130Q) - were associated with atopy risk. One SNP in IL4RA1 [rs1805010(I75V)] was associated with asthma severity, and several IL13 SNPs showed borderline significance. IL13 SNPs rs1881457(-1512) and rs1800925(-1111) were associated with better FEV(1) and FEV(1)/FVC in asthmatics. IL13 SNPs rs2066960(intron 1), rs20541(R130Q) and rs1295685(exon 4) were associated with COPD risk and lower baseline lung function in the recessive model. In females, but not in males, rs2250747 of the IL13RA1 gene was associated with COPD and lower FEV(1). Conclusion: These data suggest that IL13 SNPs (promoter and coding region) and, to a lesser extent, IL4RA SNPs may contribute to atopy and asthma. We also provide tentative evidence that IL13 SNPs in the coding region may be of significance in COPD susceptibility.