PPARβ Lentiviral Activation Particles (h): sc-400523-LAC

PPARD encodes peroxisome proliferator-activated receptor beta/delta (PPARβ), a ligand-activated nuclear receptor that heterodimerizes with RXR to regulate transcriptional programs controlling lipid utilization, fatty acid oxidation, mitochondrial energy metabolism, and cellular differentiation. PPARβ integrates metabolic and inflammatory signaling through PPAR response elements, intersecting with pathways such as AMPK, PI3K–AKT, and MAPK to modulate cell survival and stress responses. In diverse tissues, PPARD influences glucose handling, lipid homeostasis, and immune cell polarization, making it a frequent focus in studies of metabolic dysregulation, chronic inflammation, and context-dependent roles in oncogenic signaling. Altered PPARD activity has been associated with changes in oxidative metabolism, proliferative capacity, and barrier function, supporting its relevance in disease mechanism research.

PPARβ Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient PPARD upregulation across a broader range of human cell types.

PPARβ Lentiviral Activation Particles (h) 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 PPARD transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PPARβ expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native PPARD 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.