
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PGC1a Lentiviral Activation Particles (h) | sc-400070-LAC | 200 µl | $455.00 |
PPARGC1A encodes the transcriptional coactivator PGC1a, a central regulator of mitochondrial biogenesis and oxidative metabolism that coordinates nuclear respiratory factors, PPAR signaling, and antioxidant gene programs. PGC1a integrates cues from AMPK and SIRT1 to remodel energy utilization, promote fatty acid oxidation, and tune gluconeogenic and thermogenic transcriptional networks in a cell-type-dependent manner. Altered PPARGC1A activity has been linked to metabolic dysregulation, mitochondrial dysfunction, and stress responses relevant to insulin resistance, neurodegeneration, and cardiometabolic phenotypes. In human cell models, PPARGC1A is frequently studied to dissect transcriptional control of respiration, reactive oxygen species handling, and adaptive responses to nutrient and exercise-like signaling.
PGC1a 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 PPARGC1A upregulation across a broader range of human cell types.
PGC1a 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 PPARGC1A transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PGC1a expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native PPARGC1A 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.