Quick Order

Home>TNFRSF13B
Text Size:AAA

TACI/TNFRSF13B(CD267)  Protein, Antibody, ELISA Kit, cDNA Clone

TACI/TNFRSF13B(CD267) Related Area

TACI/TNFRSF13B(CD267) Related Pathways

TACI/TNFRSF13B(CD267) Related Protein, Antibody, cDNA Gene, and ELISA Kits

Featured Reagent Products

TACI/TNFRSF13B(CD267) Summary & Protein Information

TACI/TNFRSF13B(CD267) Background

Subunit structure: Binds TRAF2, TRAF5 and TRAF6. Binds the NH2-terminal domain of CAMLG with its C-terminus. {ECO:0000269|PubMed:15542592}.
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: 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. {ECO:0000269|PubMed:16007086}. Note=The disease is caused by mutations affecting the gene represented in this entry.; DISEASE: 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. {ECO:0000269|PubMed:16007086}. Note=The disease is caused by mutations affecting the gene represented in this entry.
Sequence similarity: Contains 2 TNFR-Cys repeats. {ECO:0000305}.
General information above from UniProt

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.

TACI/TNFRSF13B(CD267) Alternative Name

CVID,RYZN,TACI,CD267,CVID2,IGAD2,TNFRSF14B, [homo-sapiens]
IGAD2,RYZN, [Human]
1200009E08Rik,RP23-55I2.2,Taci,Tnfrsf13b, [mouse]
Taci,1200009E08Rik, [mus-musculus]

TACI/TNFRSF13B(CD267) Related Studies

  • Salzer U, et al. (2005) Mutations in TNFRSF13B encoding TACI are associated with common variable immunodeficiency in humans. Nat Genet. 37(8): 820-8.
  • Salzer U, et al. (2009) Relevance of biallelic versus monoallelic TNFRSF13B mutations in distinguishing disease-causing from risk-increasing TNFRSF13B variants in antibody deficiency syndromes. Blood. 113(9): 1967-76.
  • Mohammadi J, et al. (2009) Novel mutations in TACI (TNFRSF13B) causing common variable immunodeficiency. J Clin Immunol. 29(6): 777-85.
  • Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"