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Mouse Anti-TNFRSF13B Recombinant Antibody (11H3) (CBMAB-C0236-LY)

This product is antibody recognizes TNFRSF13B. The antibody 11H3 immunoassay techniques such as: IHC-F, FuncS.
See all TNFRSF13B antibodies
Published Data
Fig.1 Flow cytometry of IgG, IgA and CD27 on primary naive B cells incubated for 7 d with istoype-matched control antibody (Ctrl), anti-TACI, IL-10 and/or CpG DNA.
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Fig.2 Flow cytometry of TACI on primary CD19+CD27+ B cells from a healthy donor or a patient with CVID homozygous for a mutation resulting in the S144X TACI substitution.
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Fig.3 Immunoprecipitation, with anti-TACI or control antibody, of lysates from human primary naive B cells cultured for 15 min with medium (Ctrl) or APRIL, followed by immunoblot analysis of MyD88, TRAF2 and TACI.
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Fig.4 Confocal microscopy of TACI in primary naive B cells exposed for 15 min to APRIL.
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Summary

Host Animal
Mouse
Specificity
Human
Clone
11H3
Antibody Isotype
IgG2a
Application
IHC-F, FuncS

Basic Information

Specificity
Human
Antibody Isotype
IgG2a
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Concentration
5 μl/Test
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
TNFRSF13B Gene(Protein Coding) TNF Receptor Superfamily Member 13B
Introduction
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]
Entrez Gene ID
23495
UniProt ID
O14836
Alternative Names
TNF Receptor Superfamily Member 13B; Transmembrane Activator And CAML Interactor; TACI; Tumor Necrosis Factor Receptor Superfamily, Member 13B; Tumor Necrosis Factor Receptor Superfamily Member 13B; Tumor Necrosis Factor Receptor 13B; CD267 Antigen;
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.
Biological Process
Biological Process adaptive immune response Source:UniProtKB-KW
Biological Process B cell homeostasis Source:GO_Central1 Publication
Biological Process cell surface receptor signaling pathway Source:ProtInc1 Publication
Biological Process hematopoietic progenitor cell differentiation Source:GO_Central1 Publication
Biological Process negative regulation of B cell proliferation Source:GO_Central1 Publication
Cellular Location
Membrane
Involvement in disease
Immunodeficiency, common variable, 2 (CVID2):
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.
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.
Topology
Extracellular: 1-165
Helical: 166-186
Cytoplasmic: 187-293
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For research use only. Not intended for any clinical use.

Custom Antibody Labeling

We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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