
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
12-LO CRISPR Activation Plasmid (h) | sc-403010-ACT | 20 µg | $397.00 |
ALOX12 encodes 12-lipoxygenase (12-LO), a non-heme iron dioxygenase that converts arachidonic acid into 12(S)-hydroperoxyeicosatetraenoic acid and downstream 12-HETE lipid mediators. These eicosanoids regulate platelet activation, vascular and epithelial signaling, oxidative stress responses, and membrane remodeling, linking ALOX12 activity to inflammatory and redox-sensitive pathways. 12-LO signaling intersects with lipid peroxidation and immune modulation programs that influence cell proliferation, adhesion, and migration. Dysregulated ALOX12 expression or enzymatic flux has been associated with cardiometabolic and neuroinflammatory contexts as well as tumor-associated microenvironment biology, motivating mechanistic studies of lipid mediator networks.
12-LO CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ALOX12 expression without altering the underlying DNA sequence.
12-LO CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ALOX12 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 ALOX12 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous 12-LO expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ALOX12 locus and enabling the study of 12-LO-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of 12-LO pathway restoration in tumor cells with silenced or reduced ALOX12 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.