ACSL3 CRISPR Activation Plasmid (h): sc-403546-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACSL3 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- ACSL3 CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by ACSL3 CRISPR Activation Plasmid (h) and ACSL3 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the ACSL3 transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ACSL3 Antibody (H-9): sc-166374
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACSL3 CRISPR Activation Plasmid (h) | sc-403546-ACT | 20 µg | $397.00 |
ACSL3 (acyl-CoA synthetase long-chain family member 3) catalyzes the ATP-dependent activation of long-chain fatty acids to acyl-CoAs, a key gateway reaction that channels lipid substrates into β-oxidation, glycerolipid synthesis, and phospholipid remodeling. By controlling the availability of acyl-CoA pools at intracellular membranes, ACSL3 helps coordinate lipid droplet biogenesis, membrane composition, and metabolic flexibility under nutrient stress. ACSL3 activity is linked to pathways governing lipid homeostasis and energy metabolism, and its dysregulation has been associated with altered lipogenic programs and cellular proliferation phenotypes. These functions make ACSL3 a useful target for dissecting how fatty-acid utilization intersects with organelle dynamics and signaling networks in human cell models.
ACSL3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ACSL3 expression without altering the underlying DNA sequence.
ACSL3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ACSL3 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 ACSL3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ACSL3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ACSL3 locus and enabling the study of ACSL3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ACSL3 pathway restoration in tumor cells with silenced or reduced ACSL3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.