Pol III RPC32 Lentiviral Activation Particles (h): sc-417072-LAC
- Target species: human
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- Pol III RPC32 Lentiviral Activation Particles (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
- Pol III RPC32 Lentiviral Activation Particles (h) contain the following SAM Activation elements: a deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, an MS2-p65-HSF1 fusion protein and a target-specific 20 nt guide RNA. They also contain the blasticidin, hygromycin and puromycin resistance genes
- Upon transduction, the SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by Pol III RPC32 Lentiviral Activation Plasmid (h) and Pol III RPC32 Lentiviral Activation Plasmid (h2) target distinct regulatory regions of the POLR3G promoter. One or both designs may be available
- Following transfection, gene activation efficiency can be assayed by WB, IF or IHC using antibody: Pol III RPC32 Antibody (H-9): sc-48365
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Pol III RPC32 Lentiviral Activation Particles (h) | sc-417072-LAC | 200 µl | $455.00 | |||
Pol III RPC32 Lentiviral Activation Particles (h2) | sc-417072-LAC-2 | 200 µl | $455.00 |
POLR3G encodes Pol III RPC32, a core subunit of RNA polymerase III that supports transcription of small noncoding RNAs including tRNAs, 5S rRNA, and other regulatory RNAs essential for translation capacity, cell growth, and proteostasis. RPC32 contributes to Pol III complex assembly and promoter-dependent initiation, integrating with pathways that couple nutrient sensing and proliferative signaling to biosynthetic output. Altered Pol III activity and dysregulated small RNA production are frequently studied in the context of oncogenic transformation, cellular stress responses, and innate immune signaling triggered by cytosolic RNA species. POLR3G therefore provides a mechanistic entry point for investigating transcriptional control of noncoding RNA biogenesis and its impact on cell state decisions.
Pol III RPC32 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 POLR3G upregulation across a broader range of human cell types.
Pol III RPC32 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 POLR3G transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Pol III RPC32 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native POLR3G 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.