
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PRDM15 Lentiviral Activation Particles (h) | sc-404932-LAC | 200 µl | $455.00 |
PRDM15 (PR/SET domain 15) is a nuclear transcriptional regulator containing zinc-finger and PR/SET-related domains that support sequence-specific chromatin engagement and transcriptional control. It contributes to epigenetic regulation of gene expression programs linked to cell identity, proliferation, and developmental processes by coordinating chromatin-associated complexes at promoter and enhancer regions. Altered PRDM15 activity has been associated with dysregulated transcriptional networks and epigenomic states observed across cancer biology and developmental disorders, making it relevant for investigating lineage specification and oncogenic gene-expression dependencies. Studying PRDM15 helps define how chromatin-modifying transcription factors integrate signaling cues to shape transcriptional outputs.
PRDM15 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 PRDM15 upregulation across a broader range of human cell types.
PRDM15 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 PRDM15 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PRDM15 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native PRDM15 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.