
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACSVL6 CRISPR Activation Plasmid (h) | sc-405327-ACT | 20 µg | $397.00 |
SLC27A5 encodes ACSVL6, a very-long-chain acyl-CoA synthetase that catalyzes the ATP-dependent activation of long- and very-long-chain fatty acids to acyl-CoA thioesters, a key step that gates fatty acid utilization. By controlling acyl-CoA availability, ACSVL6 influences lipid handling processes including β-oxidation, triglyceride remodeling, and broader metabolic flux through lipid synthesis and degradation pathways. Altered fatty acid activation and acyl-CoA metabolism are linked to dysregulated lipid homeostasis, with relevance to metabolic stress states affecting liver-centric pathways and systemic energy balance. As a result, SLC27A5 is commonly studied in contexts of lipid metabolism, cellular energetic adaptation, and metabolic disease–associated signaling.
ACSVL6 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SLC27A5 expression without altering the underlying DNA sequence.
ACSVL6 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SLC27A5 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 SLC27A5 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ACSVL6 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SLC27A5 locus and enabling the study of ACSVL6-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ACSVL6 pathway restoration in tumor cells with silenced or reduced SLC27A5 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.