ATP-citrate synthase CRISPR Activation Plasmid (h): sc-403146-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATP-citrate synthase CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- ATP-citrate synthase 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 ATP-citrate synthase CRISPR Activation Plasmid (h) and ATP-citrate synthase CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the ACLY 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: ATP-citrate synthase Antibody (5F8D11): sc-517267
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ATP-citrate synthase CRISPR Activation Plasmid (h) | sc-403146-ACT | 20 µg | $397.00 | |||
ATP-citrate synthase CRISPR Activation Plasmid (h2) | sc-403146-ACT-2 | 20 µg | $397.00 |
ACLY encodes ATP-citrate synthase, a cytosolic enzyme that converts citrate and CoA into acetyl-CoA and oxaloacetate, thereby linking mitochondrial carbon flux to lipid and cholesterol biosynthesis. By supplying acetyl-CoA for fatty acid synthesis and protein acetylation, ACLY influences metabolic reprogramming, redox balance, and epigenetic regulation of gene expression. This node integrates signals from glycolysis, the TCA cycle, and nutrient-sensing pathways to shape proliferation and differentiation programs. Dysregulated ACLY activity has been associated with altered lipogenesis and acetylation landscapes observed in metabolic disease and oncology research contexts.
ATP-citrate synthase CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ACLY expression without altering the underlying DNA sequence.
ATP-citrate synthase CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ACLY 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 ACLY transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ATP-citrate synthase expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ACLY locus and enabling the study of ATP-citrate synthase-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ATP-citrate synthase pathway restoration in tumor cells with silenced or reduced ACLY expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.