
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACOX1 CRISPR Activation Plasmid (h) | sc-401690-ACT | 20 µg | $397.00 |
ACOX1 encodes acyl-CoA oxidase 1, the rate-limiting enzyme of peroxisomal straight-chain fatty acid β-oxidation that catalyzes the first oxidative step and generates hydrogen peroxide. By controlling peroxisomal lipid catabolism, ACOX1 influences cellular redox balance, lipid homeostasis, and metabolic crosstalk with mitochondrial oxidation and PPAR-regulated transcriptional programs. Altered ACOX1 activity can perturb very-long-chain fatty acid handling and peroxisome function, processes implicated in inherited peroxisomal disorders and metabolic disease phenotypes. In human cells, ACOX1 expression level is frequently used as a readout of peroxisome biogenesis, oxidative stress responses, and lipid remodeling.
ACOX1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ACOX1 expression without altering the underlying DNA sequence.
ACOX1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ACOX1 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 ACOX1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ACOX1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ACOX1 locus and enabling the study of ACOX1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ACOX1 pathway restoration in tumor cells with silenced or reduced ACOX1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.