Product nameMouse TACI Matched Antibody Pair Kit
See all TACI kits
Assay typeELISA set
Range15.6 pg/ml - 1000 pg/ml
Species reactivityReacts with: Mouse
Matched Antibody Pair kit is a titrated unlabeled capture antibody, a titrated biotin-labeled detector and a calibrated protein standard. The Matched Antibody Pair Kit can be used to quantify native and recombinant mouse TACI.
Both capture and detector antibodies are rabbit monoclonal antibodies.
Optimization of the kit reagents to sample type, immunoassay format or instrumentation may be required. Guidelines for use of this kit in a standard 96-well microplate sandwich ELISA using HRP/TMB system of colorimetric detection is described in this assay procedure for the purposes of quantification.
Additional protocol information and tips on the use of the Matched Antibody Pair kits for sandwich ELISA can be found on our website.
For additional information on the performance of the antibody pair used in this kit, please see our equivalent SimpleStep ELISA® (ab206312) which uses the same antibody pair.
Buffer information: The capture antibody is glycerol free. The detector antibody contains glycerol
To receive an electronic copy of the Certificate of Analysis, please send an email with "CoA for matched antibody pair kit" in the subject line and the desired product number and lot number in the body of the email.
Tested applicationsSuitable for: ELISAmore details
Storage instructionsStore at -20°C. Please refer to protocols.
Components 10 x 96 tests 2 x 96 tests Mouse TACI Capture Antibody 1 x 100µg 1 x 20µg Mouse TACI Detector Antibody 1 x 25µg 1 x 5µg Mouse TACI Lyophilized Protein 1 vial 1 vial
FunctionReceptor for TNFSF13/APRIL and TNFSF13B/TALL1/BAFF/BLYS that binds both ligands with similar high affinity. Mediates calcineurin-dependent activation of NF-AT, as well as activation of NF-kappa-B and AP-1. Involved in the stimulation of B- and T-cell function and the regulation of humoral immunity.
Tissue specificityHighly expressed in spleen, thymus, small intestine and peripheral blood leukocytes. Expressed in resting B-cells and activated T-cells, but not in resting T-cells.
Involvement in diseaseDefects in TNFRSF13B are the cause of immunodeficiency common variable type 2 (CVID2) [MIM:240500]. CVID2 is a primary immunodeficiency characterized by antibody deficiency, hypogammaglobulinemia, recurrent bacterial infections and an inability to mount an antibody response to antigen. The defect results from a failure of B-cell differentiation and impaired secretion of immunoglobulins; the numbers of circulating B cells is usually in the normal range, but can be low.
Defects in TNFRSF13B are a cause of immunoglobulin A deficiency 2 (IGAD2) [MIM:609529]. Selective deficiency of immunoglobulin A (IGAD) is the most common form of primary immunodeficiency, with an incidence of approximately 1 in 600 individuals in the western world. Individuals with symptomatic IGAD often have deficiency of IgG subclasses or decreased antibody response to carbohydrate antigens such as pneumococcal polysaccharide vaccine. Individuals with IGAD also suffer from recurrent sinopulmonary and gastrointestinal infections and have an increased incidence of autoimmune disorders and of lymphoid and non-lymphoid malignancies. In vitro studies have suggested that some individuals with IGAD have impaired isotype class switching to IgA and others may have a post-switch defect. IGAD and CVID have been known to coexist in families. Some individuals initially present with IGAD1 and then develop CVID. These observations suggest that some cases of IGAD and CVID may have a common etiology.
Sequence similaritiesContains 2 TNFR-Cys repeats.
- Information by UniProt
- CD 267
- CD267 antigen
SimpleStep ELISA kits
Our Abpromise guarantee covers the use of ab216786 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|ELISA||Use at an assay dependent concentration.|
ab216786 has not yet been referenced specifically in any publications.