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.
Perilipin CRISPR Activation Plasmid (h): sc-401305-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Perilipin CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Perilipin 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 Perilipin CRISPR Activation Plasmid (h) and Perilipin CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the PLIN1 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: Perilipin Antibody (G-2): sc-390169
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Perilipin CRISPR Activation Plasmid (h) | sc-401305-ACT | 20 µg | $397.00 |
PLIN1 encodes perilipin-1, a lipid droplet–associated scaffold that regulates neutral lipid storage and mobilization in adipocytes by controlling access of lipases such as ATGL and hormone-sensitive lipase to triacylglycerol. Through phosphorylation-dependent remodeling, perilipin integrates cAMP/PKA signaling with lipolytic and lipogenic programs, shaping fatty acid flux, adipocyte size, and lipid droplet dynamics. Altered PLIN1 expression or function has been linked to dysregulated adipose tissue homeostasis, insulin resistance–associated metabolic phenotypes, and lipodystrophy-like presentations, making it a relevant node in studies of adipocyte biology and systemic energy balance. In cell models, PLIN1 activity intersects with pathways governing mitochondrial substrate utilization, ER stress responses to lipid overload, and inflammatory signaling driven by ectopic lipid accumulation.
Perilipin CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PLIN1 expression without altering the underlying DNA sequence.
Perilipin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PLIN1 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 PLIN1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Perilipin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PLIN1 locus and enabling the study of Perilipin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Perilipin pathway restoration in tumor cells with silenced or reduced PLIN1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.