TNFRSF13B / TACI / CD267, Recombinant Protein

CD267, CVID, CVID2, FLJ39942, MGC133214, MGC39952, TACI, TNFRSF14B

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

Human Cells

> 90 % as determined by SDS-PAGE

Lyophilized from sterile PBS, pH 7.4

Samples are stable for up to twelve months from date of receipt at -70 degree C

Manufactured in an ISO 9001:2015 Certified Laboratory.

Small volumes of TNFRSF13B / TACI / CD267 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.

Background: Tumor necrosis factor receptor superfamily, member 13B (TNFRSF13B) also known as Transmembrane activator and CAML interactor (TACI) and CD267 antigen, is a member of the tumor necrosis factor receptor superfamily. TNFRSF13B is a trimeric cytokine receptor that binds tumor necrosis factors (TNF). The receptor cooperates with an adaptor protein which is important in determining the outcome of the response. Members of the TNF receptor superfamily (TNFRSF) have crucial roles in both innate and adaptive immunity and in cellular apoptosis process. Apoptosis is a cell suicide mechanism that enables metazoans to control cell number in tissues and to eliminate individual cells that threaten the animal's survival. Certain cells have unique sensors, termed death receptors or tumour necrosis factor (TNFR), on their surface. Tumour necrosis factors (TNFR) detect the presence of extracellular death signals and, in response, they rapidly ignite the cell's intrinsic apoptosis machinery. TACI/TNFRSF13B/CD267 induces activation of the transcription factors NFAT, AP1, and NF-kappa-B and plays a crucial role in humoral immunity by interacting with a TNF ligand.

Description: A DNA sequence encoding the human TNFRSF13B isoform 2 (O14836-2) extracellular domain (Ser 2-Thr 120) was expressed, with a polyhistidine tag at the C-terminus and a signal peptide at the N-terminus.

The recombinant human TNFRSF13B consists of 130 amino acids and has a predicted molecular mass of 14.8 kDa. In SDS-PAGE under reducing conditions, the apparent molecular mass of rhTNFRSF13B is approximately 18-24 kDa.

19,865 Da

TNF receptor superfamily member 13B

tumor necrosis factor receptor superfamily member 13B

Tumor necrosis factor receptor superfamily member 13B

TACI  [Similar Products]

The protein encoded by this gene is a lymphocyte-specific member of the tumor necrosis factor (TNF) receptor superfamily. It interacts with calcium-modulator and cyclophilin ligand (CAML). The protein induces activation of the transcription factors NFAT, AP1, and NF-kappa-B and plays a crucial role in humoral immunity by interacting with a TNF ligand. This gene is located within the Smith-Magenis syndrome region on chromosome 17. [provided by RefSeq, Jul 2008]

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.

Chromosomal Location of Human Ortholog: 17p11.2

Cellular Component: plasma membrane

Molecular Function: protein binding; receptor activity

Biological Process: B cell homeostasis; cell surface receptor linked signal transduction; hemopoietic progenitor cell differentiation; negative regulation of B cell proliferation; tumor necrosis factor-mediated signaling pathway

Disease: Immunodeficiency, Common Variable, 2; Immunoglobulin A Deficiency 2

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