Human APRIL/TNFSF13 APC-conjugated Antibody
Human APRIL/TNFSF13 APC-conjugated Antibody Summary
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Scientific Data
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Detection of APRIL/TNFSF13 in Th2-stimulated PBMCs by Flow Cytometry. Th2-stimulated peripheral blood mononuclear cells (PBMCs) were stained with Goat Anti-Human APRIL/TNFSF13 APC-conjugated Antigen Affinity-purified Polyclonal Antibody (Catalog # IC884A) and Mouse Anti-Human CD4 PE-conjugated Monoclonal Antibody (Catalog # FAB3791P). Quadrant markers were set based on control antibody staining (Catalog # IC108A). To facilitate intracellular staining, cells were fixed with Flow Cytometry Fixation Buffer (Catalog # FC004) and permeabilized with Flow Cytometry Permeabilization/Wash Buffer I (Catalog # FC005). View our protocol for Staining Intracellular Molecules.
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Preparation and Storage
- 12 months from date of receipt, 2 to 8 °C as supplied.
Background: APRIL/TNFSF13
APRIL (A Proliferation-Inducing Ligand), also known as TNFSF13, TALL2, and TRDL1, is a member of the TNF ligand superfamily (1). APRIL is synthesized as a 32 kDa type II transmembrane protein which is cleaved by furin in the Golgi to release a 17 kDa soluble molecule (2, 3). Secreted APRIL consists almost entirely of a single TNF homology domain (2, 3). Little or no transmembrane APRIL is expressed on the cell surface (3). Alternate splicing generates isoforms with short deletions at the N- or C-terminus (4). Human APRIL shares 85% aa sequence identity with mouse and rat APRIL. Among TNF superfamily ligands, BAFF shows the greatest sequence homology with APRIL, and the two proteins exhibit overlapping biological activities. APRIL promotes cellular proliferation and protects from apoptosis in normal and transformed cells (3, 5-7). It is present in elevated amounts in a wide variety of cancers primarily due to expression by tumor-infiltrating neutrophils (4, 5, 7-9). Both APRIL and BAFF bind and signal through the TNF superfamily receptors TACI and BCMA, and BAFF additionally functions through BAFF R (6, 10, 11). A stretch of basic amino acids at the N-terminus of APRIL is required for its interaction with Heparan Sulfate Proteoglycans (HSPGs) (12, 13). Binding to HSPGs is independent of APRIL’s binding to TACI and BCMA (12, 13). Interaction with HSPGs serves to concentrate APRIL on the surface of cells, thereby favoring TACI- or BCMA-mediated effects (8, 9, 13). APRIL can form bioactive heterotrimers with BAFF, and these circulate in the serum of patients with rheumatic immune disorders (14). A bioactive protein known as TWE-PRIL consists of the intracellular domain, transmembrane segment, and stalk region of TWEAK fused to the TNF homology domain of APRIL (15). TWE-PRIL is expressed in monocytes and activated T cells, and in contrast to APRIL, it is presented on the cell surface (15).
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