Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
SOAT2 CRISPR Activation Plasmid (h): sc-409713-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SOAT2 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- SOAT2 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 SOAT2 CRISPR Activation Plasmid (h) and SOAT2 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the SOAT2 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: SOAT2 Antibody (ACAT-2): sc-69837
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SOAT2 CRISPR Activation Plasmid (h) | sc-409713-ACT | 20 µg | $397.00 | |||
SOAT2 CRISPR Activation Plasmid (h2) | sc-409713-ACT-2 | 20 µg | $397.00 |
Human SOAT2 (sterol O-acyltransferase 2), also known as ACAT2, is an endoplasmic reticulum–localized enzyme that catalyzes the esterification of cholesterol with long-chain fatty acyl-CoA to form cholesteryl esters. This reaction supports intracellular cholesterol storage, lipid droplet biogenesis, and lipoprotein assembly, linking SOAT2 activity to sterol homeostasis and broader lipid metabolic networks. SOAT2 functions at the interface of cholesterol trafficking, intestinal absorption, and hepatic lipid handling, influencing pathways that govern membrane composition and neutral lipid buffering. Dysregulated cholesteryl ester metabolism and altered SOAT2 expression have been associated with metabolic and cardiovascular disease–relevant phenotypes, making it a useful target for mechanistic studies of lipid-driven cellular stress and remodeling.
SOAT2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SOAT2 expression without altering the underlying DNA sequence.
SOAT2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SOAT2 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 SOAT2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SOAT2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SOAT2 locus and enabling the study of SOAT2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SOAT2 pathway restoration in tumor cells with silenced or reduced SOAT2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.