Human TNFRSF18 ELISA Kit (GITR) (ab100527)
Key features and details
- Sensitivity: 15 pg/ml
- Range: 13.7 pg/ml - 10000 pg/ml
- Sample type: Cell culture supernatant, Plasma, Serum
- Detection method: Colorimetric
- Assay type: Sandwich (quantitative)
- Reacts with: Human
Overview
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Product name
Human TNFRSF18 ELISA Kit (GITR) -
Detection method
Colorimetric -
Sample type
Cell culture supernatant, Serum, Plasma -
Assay type
Sandwich (quantitative) -
Sensitivity
< 15 pg/ml -
Range
13.7 pg/ml - 10000 pg/ml -
Recovery
94 %
Sample specific recovery Sample type Average % Range Cell culture supernatant 95.69 84% - 105% Serum 94.18 83% - 104% Plasma 92.75 82% - 102% -
Assay duration
Multiple steps standard assay -
Species reactivity
Reacts with: Human -
Product overview
Abcam’s TNFRSF18 (GITR) Human ELISA (Enzyme-Linked Immunosorbent Assay) kit is an in vitro enzyme-linked immunosorbent assay for the quantitative measurement of Human TNFRSF18 in serum, plasma, and cell culture supernatants.
This assay employs an antibody specific for Human TNFRSF18 coated on a 96-well plate. Standards and samples are pipetted into the wells and TNFRSF18 present in a sample is bound to the wells by the immobilized antibody. The wells are washed and biotinylated anti-Human TNFRSF18 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 TNFRSF18 bound. The Stop Solution changes the color from blue to yellow, and the intensity of the color is measured at 450 nm.
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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 400X HRP-Streptavidin Concentrate 1 x 200µl 5X Assay Diluent B 1 x 15ml Assay Diluent A 1 x 30ml Biotinylated anti-Human TNFRSF18 2 vials Recombinant Human TNFRSF18 Standard (lyophilized) 2 vials Stop Solution 1 x 8ml TMB One-Step Substrate Reagent 1 x 12ml TNFRSF18 Microplate (12 x 8 wells) 1 unit -
Research areas
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Relevance
TNFRSF18 or GITR (glucocorticoid-induced TNF receptor family-regulated gene) is a 25 kD TNF receptor superfamily member (also known as AITR and TNFRSF18) originally identified in the mouse by comparing untreated and dexamethasone-treated murine T cell hybridoma cells. Human GITR was subsequently identified by searching an expressed sequence tag database. GITR is expressed on activated lymphocytes and is upregulated by T cell receptor engagement. The cytoplasmic domain of GITR is homologous to CD40, 4-1BB and CD27 and has been shown to interact with TRAF 1-3, but not TRAF 5 or 6. GITR signaling has been shown to regulate T cell proliferation and TCR-mediated apoptosis, and to break immunological self-tolerance. GITR appears to be highly expressed on CD4+CD25+ T regulatory cells and has been shown to induce NF-kB activation through TRAF2/NIK signaling. GITR has been proposed to be involved in the development of regulatory T cells and to regulate the activity of Th1 subsets. GITR binds GITRL, a TNF superfamily ligand expressed on endothelial cells, dendritic cells, macrophages, and B cells. -
Alternative names
- Activation inducible TNFR family receptor
- AITR
- GITR
see all -
Database links
- SwissProt: Q9Y5U5 Human
Images
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ELISA: ab100527 TNFRSF18 (GITR) Human ELISA Kit
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ELISA: ab100527 TNFRSF18 (GITR) Human ELISA KitGITR measured in undiluted human biological fluids (undiluted; duplicates +/- SD).
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ELISA: ab100527 TNFRSF18 (GITR) Human ELISA KitStandard curve in diluent B, with background signal subtracted (duplicates; +/- SD).
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Typical standard curveRepresentative standard curve using ab100527
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ELISA: ab100527 TNFRSF18 (GITR) Human ELISA KitStandard curve in diluent A, with background signal subtracted (duplicates; +/- SD).
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Typical standard curveRepresentative standard curve using ab100527
Datasheets and documents
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SDS download
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Datasheet download
References (0)
ab100527 has not yet been referenced specifically in any publications.