PRX2 Lentiviral Activation Particles (m): sc-422788-LAC
- Target species: mouse
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- PRX2 Lentiviral Activation Particles (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
- PRX2 Lentiviral Activation Particles (m) 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 PRX2 Lentiviral Activation Plasmid (m) and PRX2 Lentiviral Activation Plasmid (m2) target distinct regulatory regions of the Prrx2 promoter. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PRX2 Lentiviral Activation Particles (m) | sc-422788-LAC | 200 µl | $455.00 |
Mouse Prrx2 encodes the paired-related homeobox protein PRX2, a transcription factor that regulates mesenchymal cell identity and developmental programs through sequence-specific DNA binding. PRX2 influences epithelial–mesenchymal transition-like processes, cell migration, and extracellular matrix remodeling, interfacing with pathways that coordinate craniofacial, limb, and organ morphogenesis. Dysregulated PRX2-associated transcriptional networks have been linked to aberrant stromal activation and altered differentiation states relevant to fibrosis and cancer-associated mesenchymal phenotypes. In vitro, Prrx2 is commonly studied in contexts of lineage specification, wound-repair signaling, and transcriptional control of motility and matrix genes.
PRX2 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 Prrx2 upregulation across a broader range of human cell types.
PRX2 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 Prrx2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PRX2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Prrx2 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.