NP_067324.1
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NCBI GenBank Nucleotide #
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UniProt Primary Accession #
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UniProt Secondary Accession #
UniProt Related Accession #
Molecular Weight
26,947 Da
NCBI Official Full Name
tumor necrosis factor receptor superfamily member 13B
NCBI Official Synonym Full Names
tumor necrosis factor receptor superfamily, member 13b
NCBI Protein Information
tumor necrosis factor receptor superfamily member 13B
UniProt Protein Name
Tumor necrosis factor receptor superfamily member 13B
UniProt Synonym Protein Names
Transmembrane activator and CAML interactor; CD_antigen: CD267
UniProt Synonym Gene Names
UniProt Entry Name
TR13B_MOUSE
UniProt Comments for Tnfrsf13b
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: Membrane protein, integral; Cell cycle regulation; Receptor, misc.
Cellular Component: external side of plasma membrane; integral to membrane; integral to plasma membrane; membrane
Biological Process: adaptive immune response; B cell homeostasis; hemopoietic progenitor cell differentiation; immune system process; negative regulation of B cell proliferation
Disease: Immunodeficiency, Common Variable, 2
Research Articles on Tnfrsf13b
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Products associated with Tnfrsf13b elisa kit
Pathways associated with Tnfrsf13b elisa kit
Diseases associated with Tnfrsf13b elisa kit
Organs/Tissues associated with Tnfrsf13b elisa kit
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