
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PPARγ Lentiviral Activation Particles (m) | sc-422363-LAC | 200 µl | $455.00 |
Mouse Pparg encodes peroxisome proliferator-activated receptor gamma (PPARγ), a ligand-activated nuclear receptor that functions as a transcription factor governing adipocyte differentiation, lipid storage, and insulin-sensitive glucose metabolism. PPARγ heterodimerizes with RXR and binds PPAR response elements to coordinate gene programs involved in fatty acid uptake, triglyceride synthesis, and adipokine signaling. This regulator integrates nutrient and inflammatory cues, linking metabolic homeostasis to immune modulation through crosstalk with pathways such as NF-κB and MAPK. Dysregulated Pparg activity is widely studied in obesity-associated metabolic dysfunction, fatty liver phenotypes, macrophage polarization, and fibrosis-related remodeling in multiple tissues.
PPARγ Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Pparg upregulation across a broader range of human cell types.
PPARγ Lentiviral Activation Particles (m) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the Pparg transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PPARγ expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Pparg genomic locus and regulatory architecture.
The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.