
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Nrf2 CRISPR Activation Plasmid (m) | sc-421869-ACT | 20 µg | $397.00 |
Mouse Nfe2l2 encodes the transcription factor Nrf2, a master regulator of cellular redox homeostasis and xenobiotic defense. Under oxidative or electrophilic stress, Nrf2 accumulates and promotes transcription from antioxidant response elements (AREs), inducing genes involved in glutathione metabolism, NADPH regeneration, and phase II detoxification enzymes. This pathway integrates with proteostasis, mitochondrial function, and inflammatory signaling, shaping cellular responses to environmental toxicants and metabolic stress. Dysregulated Nrf2 activity has been associated with altered susceptibility to oxidative injury and inflammation, making Nfe2l2 a widely used node for modeling stress-adaptation mechanisms in disease-relevant systems.
Nrf2 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Nfe2l2 expression without altering the underlying DNA sequence.
Nrf2 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Nfe2l2 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the Nfe2l2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Nrf2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Nfe2l2 locus and enabling the study of Nrf2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Nrf2 pathway restoration in tumor cells with silenced or reduced Nfe2l2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.