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.
DGAT2 CRISPR Activation Plasmid (h): sc-416229-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DGAT2 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- DGAT2 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 DGAT2 CRISPR Activation Plasmid (h) and DGAT2 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the DGAT2 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: DGAT2 Antibody (4C1): sc-293211
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DGAT2 CRISPR Activation Plasmid (h) | sc-416229-ACT | 20 µg | $397.00 | |||
DGAT2 CRISPR Activation Plasmid (h2) | sc-416229-ACT-2 | 20 µg | $397.00 |
Human DGAT2 (diacylglycerol O-acyltransferase 2) is an endoplasmic reticulum–associated enzyme that catalyzes the final, committed step of triacylglycerol biosynthesis by acylating diacylglycerol with fatty acyl-CoA. By controlling neutral lipid production and lipid droplet biogenesis, DGAT2 links fatty acid uptake and de novo lipogenesis to cellular energy storage and membrane lipid homeostasis. DGAT2 activity intersects with lipid metabolic programs governed by SREBP signaling, β-oxidation balance, and ER stress responses during nutrient excess. Dysregulated DGAT2 expression and triglyceride accumulation are frequently studied in metabolic dysfunction, including hepatic steatosis and insulin resistance, as well as in lipid-dependent remodeling observed in certain cancers.
DGAT2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DGAT2 expression without altering the underlying DNA sequence.
DGAT2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DGAT2 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 DGAT2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DGAT2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DGAT2 locus and enabling the study of DGAT2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DGAT2 pathway restoration in tumor cells with silenced or reduced DGAT2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.