BAFF Responsive BAFF-R NF-kB Luciferase Reporter HEK293 Cell Line

The BAFF Responsive BAFF-R NF-kB Luciferase Reporter HEK293 Cell Line is a HEK293 cell line engineered to express a version of BAFFR (B-cell activating factor receptor, also known as TNFRSF13C, NM_052945.4] that is designed to couple with the canonical NF-kB (nuclear factor Kappa B) signaling pathway. The cells also express a firefly luciferase reporter driven by four copies of the NF-kappaB response element located upstream of the minimal TATA promoter. This cell line enables BAFF/BAFF-R signaling readout with a traditional luciferase reporter assay. Activation of the BAFF receptor in these cells can be monitored by measuring luciferase activity. This cell line was validated in dose-response assays using BAFF ligand, and a BAFF receptor targeting antibody Ianalumab. It was also validated with two BAFF blockers: anti-BAFF neutralizing antibody and the Dual BAFF/APRIL Antagonist, Povetacicept. Figure 1: Illustration of the mechanism by which the luciferase reporter is activated in response to BAFF binding to its receptor. Interested in screening and profiling inhibitors, blocking antibodies, or activators of BAFFR signaling without the need to purchase and license the cell line? Check out our Cell Signaling Pathway Screening. BAFF (B-cell activating factor), also known as TNFSF13B, is a member of the TNF (Tumor Necrosis Factor) super family that is produced by innate immune cells, where it undergoes furin-mediated cleavage and is released as a soluble homotrimer. BAFF influences B-cell dynamics through its interaction with three B-cell expressed receptors: BAFF-R, TACI (Transmembrane activator and CAML interactor) and BCMA (B-cell maturation antigen). While TACI and BCMA receptors also bind to the TNF super family member APRIL (A proliferation-inducing ligand), BAFF-R interacts only with BAFF ligand. Downstream signaling from BAFF/BAFF-R promotes B cell maturation and survival and has been shown to play a role in autoimmune diseases. Unique among the BAFF/APRIL family of receptors, BAFF-R preferentially signals through the non-canonical NF-kappaB pathway, making it challenging to study with existing reporter systems. Therapies targeting BAFF ligand and BAFF receptor are currently under development to treat a variety of B cell mediated autoimmune conditions including IgA nephropathy, systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).