
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PRX V Lentiviral Activation Particles (m) | sc-424925-LAC | 200 µl | $455.00 |
Mouse Prdx5 encodes peroxiredoxin V (PRX V), a thiol-dependent peroxidase that detoxifies hydrogen peroxide, organic hydroperoxides, and peroxynitrite to help maintain cellular redox homeostasis. PRX V supports antioxidant defense across compartments and contributes to preserving mitochondrial function, limiting oxidative damage to proteins and lipids, and shaping redox-sensitive signaling. Through modulation of ROS-dependent pathways, PRX V can influence inflammatory responses, stress adaptation, and apoptosis-related processes. Dysregulated Prdx5/PRX V activity has been associated with oxidative stress phenotypes relevant to neurodegeneration, metabolic dysfunction, and inflammatory tissue injury in mouse research models.
PRX V 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 Prdx5 upregulation across a broader range of human cell types.
PRX V 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 Prdx5 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PRX V expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Prdx5 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.