HEK293 RANK NFkB-Luci Cell Line
Item | Cat# | Price |
Stable Cell Line | SNB-OT-0001 | $19,800 |
Compound Testing Services | CT-001 | $1,850 per 384w plate (Up To 16 cpds Dose) |
Product Description
The RANK–RANKL signaling axis is a central regulator of bone remodeling and immune function. RANK (Receptor Activator of NF-κB) is expressed on osteoclast precursors, dendritic cells, and some immune cell subsets, while its ligand RANKL is produced by osteoblasts, stromal cells, and activated T cells. Binding of RANKL to RANK triggers recruitment of TRAF6 and activation of downstream NF-κB, MAPK, and NFATc1 pathways, driving osteoclast differentiation, survival, and bone-resorptive activity. Beyond skeletal regulation, the RANK–RANKL pathway contributes to thymic selection, lymph node organogenesis, dendritic cell maturation, and mammary gland development. Dysregulation of this axis leads to excessive osteoclast activity and is implicated in osteoporosis, rheumatoid arthritis, and cancer-associated bone disease. Therapeutically, targeting RANK–RANKL has been highly successful; the monoclonal antibody denosumab blocks RANKL and effectively suppresses osteoclast-mediated bone loss.
Screeningbio’s HEK293/RANK/NFkB-Luciferase reporter gene cell line stable expressed RANK protein and NFkB response element upstream of luciferase gene. Upon stimulated by RANKL, NFkB pathway was activated and induce luciferase expression.
Product Specifications
Target Type | RANK |
Species | Human |
HGNC Symbol | RANK |
Accession Number | NM_003839 |
Parental Line | HEK293 |
Lot# | See Vial |
Storage | Liquid Nitrogen |
Data
Target Background
Receptor activator of nuclear factor-κB (RANK) and its ligand RANKL form a critical signaling axis within the tumor necrosis factor (TNF) superfamily, regulating diverse biological processes in immunity, bone metabolism, and development. RANK is a transmembrane receptor expressed primarily on osteoclast precursors, dendritic cells, and certain epithelial cells, while RANKL is produced by osteoblasts, stromal cells, activated T cells, and other immune cell subsets. Upon binding, RANKL triggers RANK trimerization and activates downstream pathways such as NF-κB, MAPKs, and NFATc1, leading to osteoclast differentiation, survival, and functional activation. This mechanism is essential for normal bone remodeling, and its dysregulation is strongly linked to osteoporosis, bone metastases, and inflammatory bone loss.
Beyond the skeletal system, the RANK–RANKL axis plays important roles in lymph node organogenesis, mammary gland development during pregnancy, and immune cell crosstalk. In oncology, aberrant RANKL signaling has been implicated in tumor proliferation, migration, and the establishment of osteolytic lesions, making the pathway an attractive therapeutic target. The clinically approved monoclonal antibody denosumab, which inhibits RANKL, has validated the pathway’s importance in treating osteoporosis and cancer-associated bone disease. Overall, RANK–RANKL represents a versatile and clinically significant signaling system at the intersection of bone biology and immunoregulation.