TNFRSF13B; CVID; TACI; CD267; CVID2; TNFRSF14B

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

Chromosome: 17; NC_000017.11 (16939084..16972088, complement). Location: 17p11.2

Monoclonal

IgG1

(9D22)

Mouse

Protein G chromatography

Lyophilized

Stability: Lyophilized samples are stable for 2 years from date of receipt when stored at -70°C. Reconstituted antibody can be aliquoted and stored frozen at < -20 °C for at least for six months without detectable loss of activity.
Shipping: Ships with Blue Ice.

Manufactured in an ISO 9001:2008 Certified Laboratory.

Small volumes of anti-TNFRSF13B antibody 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.

TACI, transmembrane activator and CAML-interactor, is a member of the TNF receptor superfamily (TNFRSF). Within the TNFRSF, it shares the highest homology with BCMA. TACI and BCMA both bind APRIL and BLyS/BAFF, members of the TNF superfamily. TACI is expressed on the cell surface of B cells and activated, but not resting, T cells. Human and mouse TACI share 54% amino acid sequence identity.

Western Blot (WB), Immunohistochemistry (IHC) - Formalin, Neutr

IHC (frozen): 1:20 - 1:200
WB: Use at 1:500-1000
Neutralization of Ligand/receptor interaction: Yes

31,816 Da

tumor necrosis factor receptor superfamily, member 13B

tumor necrosis factor receptor superfamily member 13B; tumor necrosis factor receptor 13B; transmembrane activator and CAML interactor

Tumor necrosis factor receptor superfamily member 13B

TACI??[Similar Products]

TR13B_HUMAN

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]

Function: 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. Ref.6 Ref.7

Subunit structure: Binds TRAF2, TRAF5 and TRAF6. Binds the NH2-terminal domain of CAMLG with its C-terminus.

Subcellular location: Membrane; Single-pass type III membrane protein.

Tissue specificity: 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.

Involvement in disease: Immunodeficiency, common variable, 2 (CVID2) [MIM:240500]: 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.Note: The disease is caused by mutations affecting the gene represented in this entry. Ref.10Immunoglobulin 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.Note: The disease is caused by mutations affecting the gene represented in this entry. Ref.10

Sequence similarities: Contains 2 TNFR-Cys repeats.

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