
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACSL5 CRISPR Activation Plasmid (m) | sc-436628-ACT | 20 µg | $397.00 | |||
ACSL5 CRISPR Activation Plasmid (m2) | sc-436628-ACT-2 | 20 µg | $397.00 |
Mouse Acsl5 encodes acyl-CoA synthetase long-chain family member 5 (ACSL5), a mitochondrial-associated enzyme that activates long-chain fatty acids to acyl-CoA thioesters, committing them to β-oxidation, triglyceride synthesis, and phospholipid remodeling. By shaping acyl-CoA pools and lipid flux, ACSL5 influences mitochondrial energy metabolism, membrane composition, and lipid-mediated signaling. Altered ACSL5 activity has been linked to metabolic dysregulation, including hepatic steatosis and insulin resistance, and is frequently studied in contexts where lipid utilization and oxidative metabolism contribute to cellular stress responses.
ACSL5 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Acsl5 expression without altering the underlying DNA sequence.
ACSL5 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Acsl5 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 Acsl5 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ACSL5 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Acsl5 locus and enabling the study of ACSL5-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ACSL5 pathway restoration in tumor cells with silenced or reduced Acsl5 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.