TNFRSF13B, Recombinant Protein

TACI; Tumor necrosis factor receptor superfamily member 13B; Transmembrane activator and CAML interactor; CD267

For Research Use Only. Not for use in diagnostic procedures.

Human cells

Greater than 95% as determined by reducing SDS-PAGE.

Lyophilized from a 0.2 muM filtered solution of PBS, pH 7.4.

Lyophilized protein should be stored at -20 degree C, though stable at room temperature for 3 weeks. Reconstituted protein solution can be stored at 2-8 degree C for 2-7 days. Aliquots of reconstituted samples are stable at -20 degree C for 3 months.

Small volumes of TNFRSF13B recombinant protein vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Recombinant Mouse TNFRSF13B Protein is produced by our mammalian expression system and the target gene encoding Phe5-Thr129 is expressed with a Fc tag at the C-terminus.

ELISA (EIA),Western Blot (WB), SDS-PAGE, Mass Spectrometry (MS)

26,947 Da

tumor necrosis factor receptor superfamily, member 13b

tumor necrosis factor receptor superfamily member 13B

Tumor necrosis factor receptor superfamily member 13B

Taci  [Similar Products]

TR13B_MOUSE

TNFRSF13B: 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. Defects in TNFRSF13B are the cause of immunodeficiency common variable type 2 (CVID2). 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). 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. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Cell cycle regulation; Membrane protein, integral; Receptor, misc.

Cellular Component: external side of plasma membrane; integral to plasma membrane

Molecular Function: receptor activity

Biological Process: B cell homeostasis; cell surface receptor linked signal transduction; hemopoietic progenitor cell differentiation; negative regulation of B cell proliferation

Disease: Immunodeficiency, Common Variable, 2

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