TNFRSF13B sirna

TNFRSF13B siRNA (Human)

Cat. Num. AAA8237320

• Gene Names: TNFRSF13B; CVID; RYZN; TACI; CD267; CVID2; IGAD2; TNFRSF14B
• Reactivity: Human
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: TNFRSF13B; TNFRSF13B siRNA (Human); TACI; Tumor necrosis factor receptor superfamily member 13B; Transmembrane activator and CAML interactor; CD antigen CD267; TNFRSF13B sirna

• Host: Synthetic
• Reactivity: Human
• Specificity: TNFRSF13B siRNA (Human) is a target-specific 19-23 nt siRNA oligo duplexes designed to knock down gene expression.
• Purity/Purification: > 97%
• Form/Format: Lyophilized powder
• Sequence Length: 176

• Applicable Applications for TNFRSF13B sirna: RNA Interference (RNAi)
• Quality Control: Oligonucleotide synthesis is monitored base by base through trityl analysis to ensure appropriate coupling efficiency. The oligo is subsequently purified by affinity-solid phase extraction. The annealed RNA duplex is further analyzed by mass spectrometry to verify the exact composition of the duplex. Each lot is compared to the previous lot by mass spectrometry to ensure maximum lot-to-lot consistency.
• Directions for Use: We recommends transfection with 100 nM siRNA 48 to 72 hours prior to cell lysis. Before resuspending, briefly centrifuge the tube to ensure the lyophilized siRNA is at the bottom of the tube. Resuspend the siRNA oligos to an appropriate concentration with DEPC water. For each vial, suitable for 250 transfections in 24 well plate (20 pmol for each well).
• Components: We offer pre-designed sets of 3 different target-specific siRNA oligo duplexes of human TNFRSF13B gene. Each vial contains 5 nmol of lyophilized siRNA. The duplexes can be transfected individually or pooled together to achieve knockdown of the target gene, which is most commonly assessed by qPCR or western blot. Our siRNA oligos are also chemically modified (2'-OMe) at no extra charge for increased stability and enhanced knockdown in vitro and in vivo.
• Preparation and Storage: Shipped at 4 degree C. Store at -20 degree C for one year.

Related Product Information for TNFRSF13B sirna

siRNA to inhibit TNFRSF13B expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 6912694
• NCBI GeneID: 23495
• NCBI Accession #: NP_036584.1
• NCBI GenBank Nucleotide #: NM_012452.2
• UniProt Accession #: O14836; Q32LX4; Q7Z6F5; B2R8B0; B7Z6V8
• Molecular Weight: 19,865 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 Official Symbol: TNFRSF13B
• NCBI Official Synonym Symbols: CVID; RYZN; TACI; CD267; CVID2; IGAD2; TNFRSF14B
• NCBI Protein Information: tumor necrosis factor receptor superfamily member 13B
• UniProt Protein Name: Tumor necrosis factor receptor superfamily member 13B
• Protein Family: Tumor necrosis factor receptor superfamily
• UniProt Gene Name: TNFRSF13B
• UniProt Synonym Gene Names: TACI
• UniProt Entry Name: TR13B_HUMAN

NCBI Description

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]

Uniprot Description

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: Cell cycle regulation; Receptor, misc.; Membrane protein, integral

Chromosomal Location of Human Ortholog: 17p11.2

Cellular Component: integral to plasma membrane; external side of plasma membrane

Molecular Function: protein binding; receptor activity

Biological Process: cell surface receptor linked signal transduction; B cell homeostasis; hemopoietic progenitor cell differentiation; negative regulation of B cell proliferation

Disease: Immunodeficiency, Common Variable, 2; Immunoglobulin A Deficiency 2