• Target：
• CD267

• Fields：
• >>Cytokine-cytokine receptor interaction;>>Intestinal immune network for IgA production;>>Primary immunodeficiency

• Gene Name：
• TNFRSF13B

• Protein Name：
• Tumor necrosis factor receptor superfamily member 13B

• Human Gene Id：
• 23495

• Human Swiss Prot No：
• O14836

• Mouse Gene Id：
• 57916

• Mouse Swiss Prot No：
• Q9ET35

• Immunogen：
• The antiserum was produced against synthesized peptide derived from the Internal region of human TNFRSF13B. AA range:81-130

• Specificity：
• CD267 Polyclonal Antibody detects endogenous levels of CD267 protein.

• Formulation：
• Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.

• Source：
• Polyclonal, Rabbit,IgG

• Dilution：
• WB 1:500 - 1:2000. ELISA: 1:10000. Not yet tested in other applications.

• Purification：
• The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.

• Concentration：
• 1 mg/ml

• Storage Stability：
• -15°C to -25°C/1 year(Do not lower than -25°C)

• Other Name：
• TNFRSF13B;TACI;Tumor necrosis factor receptor superfamily member 13B;Transmembrane activator and CAML interactor;CD267

• Observed Band(KD)：
• 32kD

• Background：
• 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：
• disease:Defects in TNFRSF13B are a cause of common variable immunodeficiency (CVID) [MIM:240500]. CVID is characterized by a deficiency in all immunoglobulin (Ig) isotypes. Individuals with CVID suffer from recurrent sinopulmonary and gastrointestinal infections and have an increased incidence of autoimmune disorders and of lymphoid and non-lymphoid malignancies. There is evidence for a global isotype switching defect in some individuals with CVID. But CVID is a complex and heterogeneous disease in which defects in B-cell survival, number of circulating CD27+ memory B-cells (including IgM+CD27+ B-cells), B-cell activation after antigen receptor cross-linking, T-cell signaling and cytokine expression have been observed.,disease: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

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

• Expression：
• 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.

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