The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
< 0.100 Eu/µg
% SDS-PAGE. ab50090 purity was assessed also by HPLC.
Endotoxin level is less than 0.1 ng per µg (1EU/µg).
Soluble TACI inhibits APRIL-stimulated proliferation of primary B-cells by blocking the binding of APRIL to the membrane anchored TACI receptor.
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Shipped at 4°C. The lyophilized protein is stable for a few weeks at room temperature. Store at -20°C long term.
Reconsitute to 1mg/ml in distilled water.
Transmembrane activator and CAML interactor
Tumor necrosis factor receptor 13B
Tumor necrosis factor receptor superfamily member 13B
Receptor 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.
Highly 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.
Defects 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.