
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ADRP CRISPR Activation Plasmid (h) | sc-400802-ACT | 20 µg | $397.00 |
PLIN2 encodes adipose differentiation-related protein (ADRP), a lipid droplet–associated perilipin that coats neutral lipid stores and regulates their stability, turnover, and access by lipases. ADRP helps coordinate intracellular triglyceride and cholesteryl ester handling, linking lipid droplet biogenesis to cellular energy balance, oxidative stress responses, and metabolic signaling. Altered PLIN2 expression is associated with lipid accumulation phenotypes observed in metabolic dysfunction and inflammatory states, and it is frequently studied in contexts of hepatic steatosis, atherosclerotic foam cell formation, and tumor lipid metabolism. As a readout of lipid storage dynamics, ADRP is widely used to interrogate pathways controlling fatty acid uptake, esterification, and lipophagy.
ADRP CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PLIN2 expression without altering the underlying DNA sequence.
ADRP CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PLIN2 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 PLIN2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ADRP expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PLIN2 locus and enabling the study of ADRP-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ADRP pathway restoration in tumor cells with silenced or reduced PLIN2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.