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

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cell lysates, serum, plasma
Species Reactivity
Intended Use
The Human CD23 ELISA Kit contains the components necessary for quantitative determination of natural or recombinant Human CD23 concentrations within any experimental sample including cell lysates, serum and plasma.
Contents of Kit
1. Microstrips Coated w/ Capture Antibody: 12 x 8-Well Microcstrips
2. Protein Standard: Lyophilized (9.2 ng), Red
3. Biotinylated Detection Antibody: Lyophilized, Yellow
4. 400x Streptavidin-HRP: 30 μL, Blue
5. Wash Buffer (10x): 50 mL, Clear
6. Assay Diluent: 50 mL, Clear
7. Ready-to-Use Substrate: 12 mL, Brown
8. Stop Solution: 12 mL, Clear
9. Adheive Plate Sealers: 4 Seets
10. Technical Manual: 1 Manual
4°C/6 Months
Detection Range
16-1000 pg/mL
The Human CD23 ELISA Kit allows for the detection and quantification of endogenous levels of natural and/or recombinant Human CD23 proteins within the range of 16-1000 pg/mL.
Standard Curve


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Genome-wide interaction study reveals age-dependent determinants of responsiveness to inhaled corticosteroids in individuals with asthma


Authors: Dahlin, Amber; Sordillo, Joanne E.; McGeachie, Michael; Kelly, Rachel S.; Tantisira, Kelan G.; Lutz, Sharon M.; Lasky-Su, Jessica; Wu, Ann Chen

While genome-wide association studies have identified genes involved in differential treatment responses to inhaled corticosteroids (ICS) in asthma, few studies have evaluated the potential effects of age in this context. A significant proportion of asthmatics experience exacerbations (hospitalizations and emergency department visits) during ICS treatment. We evaluated the interaction of genetic variation and age on ICS response (measured by the occurrence of exacerbations) through a genome-wide interaction study (GWIS) of 1,321 adult and child asthmatic patients of European ancestry. We identified 107 genome-wide suggestive (P<10(-05)) age-by-genotype interactions, two of which also met genome-wide significance (P<5x10(-08)) (rs34631960 [OR 2.3 +/- 1.6-3.3] in thrombospondin type 1 domain-containing protein 4 (THSD4) and rs2328386 [OR 0.5 +/- 0.3-0.7] in human immunodeficiency virus type I enhancer binding protein 2 (HIVEP2)) by joint analysis of GWIS results from discovery and replication populations. In addition to THSD4 and HIVEP2, age-by-genotype interactions also prioritized genes previously identified as asthma candidate genes, including DPP10, HDAC9, TBXAS1, FBXL7, and GSDMB/ORMDL3, as pharmacogenomic loci as well. This study is the first to link these genes to a pharmacogenetic trait for asthma.

Epstein-barr virus infected gastric adenocarcinoma expresses latent and lytic viral transcripts and has a distinct human gene expression profile


Authors: Tang, Weihua; Morgan, Douglas R.; Meyers, Michael O.; Dominguez, Ricardo L.; Martinez, Enrique; Kakudo, Kennichi; Kuan, Pei Fen; Banet, Natalie; Muallem, Hind; Woodward, Kimberly; Speck, Olga; Gulley, Margaret L.

Background: EBV DNA is found within the malignant cells of 10% of gastric cancers. Modern molecular technology facilitates identification of virus-related biochemical effects that could assist in early diagnosis and disease management. Methods: In this study, RNA expression profiling was performed on 326 macrodissected paraffin-embedded tissues including 204 cancers and, when available, adjacent non-malignant mucosa. Nanostring nCounter probes targeted 96 RNAs (20 viral, 73 human, and 3 spiked RNAs). Results: In 182 tissues with adequate housekeeper RNAs, distinct profiles were found in infected versus uninfected cancers, and in malignant versus adjacent benign mucosa. EBV-infected gastric cancers expressed nearly all of the 18 latent and lytic EBV RNAs in the test panel. Levels of EBER1 and EBER2 RNA were highest and were proportional to the quantity of EBV genomes as measured by Q-PCR. Among protein coding EBV RNAs, EBNA1 from the Q promoter and BRLF1 were highly expressed while EBNA2 levels were low positive in only 6/14 infected cancers. Concomitant upregulation of cellular factors implies that virus is not an innocent bystander but rather is linked to NFKB signaling (FCER2, TRAF1) and immune response (TNFSF9, CXCL11, IFITM1, FCRL3, MS4A1 and PLUNC), with PPARG expression implicating altered cellular metabolism. Compared to adjacent non-malignant mucosa, gastric cancers consistently expressed INHBA, SPP1, THY1, SERPINH1, CXCL1, FSCN1, PTGS2 (COX2), BBC3, ICAM1, TNFSF9, SULF1, SLC2A1, TYMS, three collagens, the cell proliferation markers MYC and PCNA, and EBV BLLF1 while they lacked CDH1 (E-cadherin), CLDN18, PTEN, SDC1 (CD138), GAST (gastrin) and its downstream effector CHGA (chromogranin). Compared to lymphoepithelioma-like carcinoma of the uterine cervix, gastric cancers expressed CLDN18, EPCAM, REG4, BBC3, OLFM4, PPARG, and CDH17 while they had diminished levels of IFITM1 and HIF1A. The druggable targets ERBB2 (Her2), MET, and the HIF pathway, as well as several other potential pharmacogenetic indicators (including EBV infection itself, as well as SPARC, TYMS, FCGR2B and REG4) were identified in some tumor specimens. Conclusion: This study shows how modern molecular technology applied to archival fixed tissues yields novel insights into viral oncogenesis that could be useful in managing affected patients.

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