PIWIL2 Lentiviral Activation Particles (h): sc-402211-LAC
- Target species: human
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- PIWIL2 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
- PIWIL2 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 PIWIL2 Lentiviral Activation Plasmid (h) and PIWIL2 Lentiviral Activation Plasmid (h2) target distinct regulatory regions of the PIWIL2 promoter. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PIWIL2 Lentiviral Activation Particles (h) | sc-402211-LAC | 200 µl | $455.00 |
PIWIL2 encodes a PIWI family Argonaute protein that binds piRNAs to regulate small RNA–guided gene silencing, supporting transposon repression, genome stability, and epigenetic control of transcription. In human cells, PIWIL2 is linked to RNA processing, chromatin-associated regulation, and maintenance of germline-associated programs, with emerging roles in stem-like states and cellular differentiation. Dysregulated PIWIL2 expression has been reported across multiple tumor contexts and is frequently studied in relation to proliferation, invasion, and altered cell fate signaling. As a result, PIWIL2 is a useful target for investigating piRNA pathway biology, non-coding RNA regulation, and mechanisms that couple genome surveillance to oncogenic phenotypes.
PIWIL2 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 PIWIL2 upregulation across a broader range of human cell types.
PIWIL2 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 PIWIL2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PIWIL2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native PIWIL2 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.