RANK/NF-κB Luciferase Reporter HEK293 Cell Line
RANK/NF-κB Luciferase Reporter HEK293 Cell Line is a HEK293 cell line expressing the firefly luciferase reporter under the control of Nuclear factor-κB (NF-κB) Response Elements and with constitutive expression of human RANK (Receptor activator of nuclear factor-κB; TNFRSF11A; ref. seq. NM_003839.2). Overexpression of RANK was confirmed by flow cytometry and the cell line was functionally validated for its response to RANK ligand (RANKL), anti-RANKL antibody and IKK-16.
Figure 1: Activation of NF-κB-dependent luciferase reporter in the RANK/NF-κB Luciferase Reporter HEK293 Cell Line.
Interested in screening and profiling inhibitors, blocking antibodies, or activators of RANK without the need to purchase and license the cell line? Check out our Cell Signaling Pathway Screening.
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Materials Required for Cell Culture
| Name | Ordering Information |
| Thaw Medium 1 | BPS Bioscience #60187 |
| Growth Medium 1G | BPS Bioscience #79544 |
Materials Required for Cellular Assay
| Name | Ordering Information |
| Human RANKL | R&D Systems #390-TN-010 |
| Anti-RANKL Neutralizing Antibody | BPS Bioscience #100874 |
| IKK-16 dihydrochloride | Sigma #SML1138 |
| ONE-Step™ Luciferase Assay System | BPS Bioscience #60690 |
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The cell line has been screened to confirm the absence of Mycoplasma species.
Bone homeostasis relies on the balance between bone formation by osteoblasts and bone resorption by osteoclasts. Appropriate signaling between the two cell types is necessary to maintain bone health. Osteoblasts express RANKL (receptor activator of NF-κB ligand), which binds to the receptor RANK on the surface of osteoclasts. This results in activation of the NF-κB pathway to promote osteoclast survival and proliferation, leading to the resorption of bone. This mechanism is tempered by osteoblast-mediated secretion of OPG (osteoprotegerin) which competes with RANKL for binding to RANK and protects from excessive bone resorption. Therefore, abnormal production of RANKL or OPG can cause osteoporosis and other bone-related disorders. This pathway is also dysregulated by bone-colonizing tumor cells in the first steps of metastasis, making the RANKL/RANK signaling pathway a valuable target for drug discovery and development.
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