
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACOT11 CRISPR Activation Plasmid (m) | sc-435977-ACT | 20 µg | $397.00 |
Acot11 encodes acyl-CoA thioesterase 11 (ACOT11), a mitochondrial lipid-metabolic enzyme that hydrolyzes long-chain fatty acyl-CoAs to free fatty acids and CoA, thereby shaping acyl-CoA pool size and downstream β-oxidation flux. By modulating mitochondrial substrate availability and lipid signaling intermediates, ACOT11 influences energy balance, oxidative metabolism, and adipose tissue lipid handling. In mouse systems, altered ACOT11 activity has been linked to metabolic phenotypes involving thermogenesis and nutrient utilization, making it relevant for studying mitochondrial function, fatty acid homeostasis, and metabolic stress responses.
ACOT11 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Acot11 expression without altering the underlying DNA sequence.
ACOT11 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Acot11 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 Acot11 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ACOT11 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Acot11 locus and enabling the study of ACOT11-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ACOT11 pathway restoration in tumor cells with silenced or reduced Acot11 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.