
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACAT-1 CRISPR Activation Plasmid (h) | sc-402300-ACT | 20 µg | $397.00 |
ACAT1 encodes ACAT-1, a mitochondrial thiolase (acetyl-CoA acetyltransferase 1) that catalyzes reversible thiolysis of acetoacetyl-CoA, linking ketone body utilization with acetyl-CoA supply for oxidative metabolism. This enzyme participates in mitochondrial lipid and amino acid catabolism and supports energy homeostasis by channeling substrates into the TCA cycle. Altered ACAT-1 activity has been associated with inborn errors of ketone body metabolism and broader mitochondrial dysfunction phenotypes. ACAT1 is therefore frequently studied in metabolic remodeling, nutrient stress responses, and mitochondrial pathway crosstalk relevant to neurodegeneration and cancer cell bioenergetics.
ACAT-1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ACAT1 expression without altering the underlying DNA sequence.
ACAT-1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ACAT1 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 ACAT1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ACAT-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ACAT1 locus and enabling the study of ACAT-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ACAT-1 pathway restoration in tumor cells with silenced or reduced ACAT1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.