NF- κB Reporter (Luc) – THP-1 Cell Line
NF-κB reporter (Luc)-THP-1 Cell Line is a THP-1 cell line designed for monitoring NF-κB (nuclear factor κB) signal transduction pathways. It contains a firefly luciferase reporter driven by four copies of the NF-κB response element located upstream of the minimal TATA promoter. After activation by pro-inflammatory cytokines or NOD agonists, endogenous NF-κB transcription factors bind to the DNA response elements, inducing transcription of the luciferase reporter.
Interested in screening and profiling inhibitors, blocking antibodies, or activators of NF-κB-mediated signaling without the need to purchase and license the cell line? Check out our Cell Signaling Pathway Screening.
Purchase of this cell line is for research purposes only; commercial use requires a separate license. View the full terms and conditions.
Materials Required for Cell Culture
Name | Ordering Information |
Thaw Medium 8 | BPS Bioscience #79652 |
Growth Medium 8A | BPS Bioscience #79653 |
Materials Required for Cellular Assay
Name | Ordering Information |
Recombinant Human hTNFα | R&D Systems #210-TA |
LPS-EK (TLR4 and TLR2 agonist) | Invivogen #tlrl-eklps |
L18-MDP (NOD2 agonist) | Invivogen #tlrl-lmdp |
Recombinant Human IL-1 beta/IL-1F2 Protein | R&D Systems #201-LB |
IKK-16 dihydrochloride | Sigma #SML1138 |
Assay Medium: Thaw Medium 8 | BPS Bioscience #79652 |
96-well tissue culture-treated white clear-bottom assay plate | Corning #3610 |
ONE-Step™ luciferase assay system | BPS Bioscience #60690 |
Luminometer |
The cell line has been screened to confirm the absence of Mycoplasma species.
The role of NF-κB (nuclear factor-κB) activation is well-characterized in canonical (classical) and noncanonical (alternative)
signaling pathways of inflammation. Two major forms of innate immune sensors are Toll-like receptors (TLR) and NOD/CATERPILLER proteins. Mutations in NOD2 (nucleotide-binding oligomerization domain-containing protein 2) have been linked to chronic autoinflammatory and autoimmune diseases, such as Crohn’s disease and Blaus syndrome. Studying the canonical and noncanonical NF-κB pathways and the influence of TLR pathways and NOD2 mutations can further our understanding of autoimmune regulation.
Pessara U. and Koch N., 1990 Mol Cell Biol. 10(8):4146-4154.
Baeuerle P.A., 1998 Curr Biol. 8(1):R19-R22.
Pan, Q., et al., 2006 Infection and Immunity, 74(4), 2121–2127.