TACR3 (NK3R) / NFAT Luciferase Reporter HEK293 Cell Line

TACR3 (NK3R)/NFAT Luciferase Reporter HEK293 Cell Line is a HEK293 cell line stably expressing full-length human Tachykinin Receptor 3 (TACR3, also known as neurokinin receptor NK3R or HH11, accession number: NM_001059.2), and a firefly luciferase reporter under the control of NFAT (nuclear factor of activated T cells) response element. This cell line was validated for its responses to Tachykinin Receptor 3 ligand (Neurokinin B), the selective agonist Senktide, and the selective antagonist SB 222200. Figure 1: Illustration of the mechanism by which the luciferase reporter is activated is response to TACR3 agonists.Interested in screening and profiling molecules targeting GPR52 signaling without the need to purchase and license the cell line? Check out our Cell Signaling Pathway Screening. Tachykinins are a family of neuropeptides that act as neurotransmitters and signaling molecules, regulating pain transmission, inflammation, smooth muscle contraction, and neuroimmune responses. The best-characterized tachykinins, including substance P, neurokinin A, and neurokinin B, exert their effects by binding to neurokinin receptors (NK1R, NK2R, and NK3R) expressed in the nervous, immune, and cardiovascular systems.Neurokinin receptors belong to the family of G protein-coupled receptors (GPCR). Neurokinin receptors couple to G-proteins Gq/11 and Galphas, activating the PLC-Gq signaling pathway and triggering a spike in intracellular calcium Ca2+. Neurokinins play a role in smooth muscle contraction, secretion, proliferation, and nociception. They also contribute to inflammatory bowel disease (IBD), rheumatoid arthritis (RA), multiple sclerosis (MS), psoriasis, and cancer. Neurokinin B (NKB) signaling via its cognate receptor, neurokinin 3 receptor (NK3R) in the hypothalamus is a mediator of menopausal vasomotor symptoms (VMS). NK3R antagonists have been developed targeting the NKB signaling pathway as a novel effective non-hormonal therapeutic option for menopausal VMS.