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GAL4-DBD-PPARγ-LBD-BSD
$595.00 – $2,395.00
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FOXA1/2 Reporter Lentivirus
$595.00
GAL4-DBD-NR1D1-LBD-VP16-BSD
$595.00 – $2,395.00
REV-ERB Alpha (REV-ERBα), part of the nuclear receptor subfamily 1 group D member 1 (NR1D1), is a critical regulator of the circadian clock, maintaining rhythmic control by repressing positive clock elements. This nuclear receptor plays a pivotal role in synchronizing physiological processes, including metabolism and immune function. The gene encoding REV-ERBα demonstrates circadian patterns, with predominant expression in metabolic tissues such as skeletal muscle, liver, adipose tissue, and the brain.
As a repressor, REV-ERBα modulates the expression of target genes under circadian control, influencing lipid metabolism, glucose homeostasis, and inflammatory responses. This receptor is crucial for maintaining metabolic homeostasis in response to environmental cues, making it a valuable target in studies of circadian biology and metabolic disorders.
The GAL4-DBD-REV-ERBα LBD fusion construct is designed to monitor REV-ERBα activity, offering researchers a powerful tool for studying ligand interactions with this nuclear receptor. With high-titer lentiviral particles and flexible readout options (e.g., GFP, RFP, or Firefly Luciferase), this system facilitates the creation of stable cell lines, eliminating the need for repeated transfections—resulting in cost savings and reproducible results. For custom solutions featuring alternative nuclear receptor family members, we offer similar pricing and a streamlined production timeline.
Contact us today to see how this tool can accelerate your drug discovery pipeline and therapeutic research.
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Details
The GAL4-DBD-NR1D1-LBD-VP16-BSD construct is designed to measure the activity of the REV-ERBα (NR1D1) receptor, a key regulator of circadian rhythm and metabolic pathways. This construct utilizes a fusion of the GAL4 DNA-binding domain (DBD), the NR1D1 ligand-binding domain (LBD), and a VP16 activation domain. The GAL4 DBD binds to a specific DNA sequence in the 5x GAL4 UAS-TAG-Puro construct, which contains a target sequence upstream of a reporter gene. When transcription is active, the reporter gene produces a measurable signal (visualized as GFP fluorescence), providing a direct readout of REV-ERBα activity. Similarly, the GAL4-DBD-NR1D1-LBD-VP16-BSD construct can instead be combined with the GAL4-TAR-Puro reporter construct (expresses RFP as the readout) or GAL4-TAL-Puro (expresses Firefly Luc as the readout) for flexibility in experimental readouts.
Experimental Data and Interpretation
HEK293 cells co-transfected with GAL4-DBD-NR1D1-LBD-VP16-BSD and GAL4-TAG-Puro constructs were treated with DMSO (control), SR9011 (agonist), or SR8278 (antagonist) to illustrate NR1D1’s behavior under different conditions:
- DMSO (Control): Shows baseline fluorescence, establishing a reference level for transcriptional activity without any ligand influence.
- SR9011 (Agonist): This ligand activates REV-ERBα, leading to suppressed transcription of the reporter gene, resulting in reduced fluorescence. This suppression is consistent with REV-ERBα’s role as a transcriptional repressor when activated.
- SR8278 (Antagonist): As an antagonist, SR8278 blocks REV-ERBα’s activity, preventing its repressive effects on transcription. This leads to increased fluorescence, demonstrating that blocking REV-ERBα allows transcriptional activation.
Application and Research Utility
This construct provides researchers with a sensitive tool for studying the activity of REV-ERBα (NR1D1) in real-time. By monitoring changes in fluorescence in response to specific agonists and antagonists, researchers can investigate REV-ERBα’s role in circadian regulation, metabolism, and immune response. The ability to modulate and measure NR1D1 activity is invaluable for exploring the pathways controlled by this receptor and identifying potential therapeutic targets within circadian and metabolic research.
This product is supplied as pre-packaged lentiviral particles only. Plasmids are not available for this product.