Human IL-1 beta ELISA Kit (ab100562)
Key features and details
- Sensitivity: 0.3 pg/ml
- Range: 0.48 pg/ml - 100 pg/ml
- Sample type: Cell culture supernatant, Plasma
- Detection method: Colorimetric
- Assay type: Sandwich (quantitative)
- Reacts with: Human
Overview
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Product name
Human IL-1 beta ELISA Kit
See all IL-1 beta kits -
Detection method
Colorimetric -
Sample type
Cell culture supernatant, Plasma -
Assay type
Sandwich (quantitative) -
Sensitivity
< 0.3 pg/ml -
Range
0.48 pg/ml - 100 pg/ml -
Recovery
99 %
Sample specific recovery Sample type Average % Range Cell culture supernatant 100.43 89% - 110% Plasma 99.66 90% - 107% -
Assay duration
Multiple steps standard assay -
Species reactivity
Reacts with: Human -
Product overview
Human IL-1 beta ELISA (Enzyme-Linked Immunosorbent Assay) kit is an in vitro enzyme-linked immunosorbent assay for the quantitative measurement of human IL-1 beta in plasma and cell culture supernatants. (Human IL-1 beta concentration is quite low in normal plasma, it may not be detected in this assay).
This assay employs an antibody specific for human IL-1 beta coated on a 96-well plate. Standards and samples are pipetted into the wells and IL-1 beta present in a sample is bound to the wells by the immobilized antibody. The wells are washed and biotinylated anti-Human IL-1 beta antibody is added. After washing away unbound biotinylated antibody, HRP-conjugated streptavidin is pipetted to the wells. The wells are again washed, a TMB substrate solution is added to the wells and color develops in proportion to the amount of IL-1 beta bound. The Stop Solution changes the color from blue to yellow, and the intensity of the color is measured at 450 nm.
We have not been able to detect the endogenous human IL-1 beta in normal serum with ab100562, only in serum spiked with human IL-1 beta.
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Notes
Optimization may be required with urine samples.
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Platform
Microplate
Properties
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Storage instructions
Store at -20°C. Please refer to protocols. -
Components 1 x 96 tests 20X Wash Buffer 1 x 25ml 300X HRP-Streptavidin Concentrate 1 x 200µl 5X Assay Diluent B 1 x 15ml Assay Diluent A 1 x 30ml Biotinylated anti-Human IL-1 beta 2 vials IL-1 beta Microplate (12 x 8 wells) 1 unit Recombinant Human IL-1 beta Standards (lyophilized) 2 vials Stop Solution 1 x 8ml TMB One-Step Substrate Reagent 1 x 12ml -
Research areas
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Function
Potent proinflammatory cytokine. Initially discovered as the major endogenous pyrogen, induces prostaglandin synthesis, neutrophil influx and activation, T-cell activation and cytokine production, B-cell activation and antibody production, and fibroblast proliferation and collagen production. Promotes Th17 differentiation of T-cells. -
Tissue specificity
Expressed in activated monocytes/macrophages (at protein level). -
Sequence similarities
Belongs to the IL-1 family. -
Post-translational
modificationsActivation of the IL1B precursor involves a CASP1-catalyzed proteolytic cleavage. Processing and secretion are temporarily associated. -
Cellular localization
Cytoplasm, cytosol. Lysosome. Secreted, exosome. Cytoplasmic vesicle, autophagosome. Secreted. The precursor is cytosolic. In response to inflammasome-activating signals, such as ATP for NLRP3 inflammasome or bacterial flagellin for NLRC4 inflammasome, cleaved and secreted. IL1B lacks any known signal sequence and the pathway(s) of its secretion is(are) not yet fully understood (PubMed:24201029). On the basis of experimental results, several unconventional secretion mechanisms have been proposed. 1. Secretion via secretory lysosomes: a fraction of CASP1 and IL1B precursor may be incorporated, by a yet undefined mechanism, into secretory lysosomes that undergo Ca(2+)-dependent exocytosis with release of mature IL1B (PubMed:15192144). 2. Secretory autophagy: IL1B-containing autophagosomes may fuse with endosomes or multivesicular bodies (MVBs) and then merge with the plasma membrane releasing soluble IL1B or IL1B-containing exosomes (PubMed:24201029). However, autophagy impacts IL1B production at several levels and its role in secretion is still controversial. 3. Secretion via exosomes: ATP-activation of P2RX7 leads to the formation of MVBs containing exosomes with entrapped IL1B, CASP1 and other inflammasome components. These MVBs undergo exocytosis with the release of exosomes. The release of soluble IL1B occurs after the lysis of exosome membranes (By similarity). 4. Secretion by microvesicle shedding: activation of the ATP receptor P2RX7 may induce an immediate shedding of membrane-derived microvesicles containing IL1B and possibly inflammasome components. The cytokine is then released in the extracellular compartment after microvesicle lysis (PubMed:11728343). 5. Release by translocation through permeabilized plasma membrane. This may occur in cells undergoing pyroptosis due to sustained activation of the inflammasome (By similarity). These mechanisms may not be not mutually exclusive. - Information by UniProt
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Alternative names
- Catabolin
- H1
- IFN beta inducing factor
see all -
Database links
- Entrez Gene: 3553 Human
- Omim: 147720 Human
- SwissProt: P01584 Human
- Unigene: 126256 Human
Images
Datasheets and documents
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SDS download
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Datasheet download
References (44)
ab100562 has been referenced in 44 publications.
- Liu J et al. Study on Toll-Like Receptor 2-Mediated Inflammation-Induced Familial Hypertension Combined with Hyperlipemia and Its Mechanism. J Healthc Eng 2022:1473597 (2022). PubMed: 35035808
- Niu F et al. Histone demethylase KDM5A regulates the functions of human periodontal ligament stem cells during periodontitis via the miR-495-3p/HOXC8 axis. Regen Ther 20:95-106 (2022). PubMed: 35509266
- Sun W et al. Diagnostic value of lncRNA NORAD in pulmonary tuberculosis and its regulatory role in Mycobacterium tuberculosis infection of macrophages. Microbiol Immunol 66:433-441 (2022). PubMed: 35568971
- Peipei W et al. Sevoflurane ameliorates LPS-induced inflammatory injury of HK-2 cells through Sirtuin1/NF-?B pathway. Allergol Immunopathol (Madr) 50:115-123 (2022). PubMed: 35789410
- Qian X & Yang L ROCK2 knockdown alleviates LPS-induced inflammatory injury and apoptosis of renal tubular epithelial cells via the NF-?B/NLRP3 signaling pathway. Exp Ther Med 24:603 (2022). PubMed: 35949322