
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PPARγ CRISPR Activation Plasmid (m) | sc-422363-ACT | 20 µg | $397.00 |
Mouse Pparg encodes peroxisome proliferator-activated receptor gamma (PPARγ), a ligand-activated nuclear receptor that functions as a transcriptional regulator of lipid handling, adipocyte differentiation, and glucose homeostasis. PPARγ integrates metabolic cues to control gene programs involved in fatty acid uptake and storage, adipokine signaling, mitochondrial function, and inflammatory tone through crosstalk with insulin/PI3K-AKT, AMPK, and NF-κB-associated pathways. Altered Pparg activity is widely used as a mechanistic entry point for studying metabolic dysregulation, adipose tissue remodeling, and inflammatory phenotypes in mouse cellular systems.
PPARγ CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Pparg expression without altering the underlying DNA sequence.
PPARγ CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Pparg 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 Pparg transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PPARγ expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Pparg locus and enabling the study of PPARγ-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PPARγ pathway restoration in tumor cells with silenced or reduced Pparg expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.