
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Prickle4 Lentiviral Activation Particles (h) | sc-412059-LAC | 200 µl | $455.00 |
PRICKLE4 encodes Prickle4, a conserved regulator of planar cell polarity signaling that helps coordinate directional cell behaviors by modulating non-canonical Wnt/PCP pathway activity. Through interactions with core PCP components and downstream cytoskeletal regulators, Prickle4 can influence cell polarity, adhesion, and motility, processes relevant to tissue organization and morphogenesis. Altered PCP signaling is implicated in developmental abnormalities and cancer-associated phenotypes such as aberrant migration and invasion, making PRICKLE4 a useful node for mechanistic pathway studies. In human cell models, interrogating PRICKLE4 expression and downstream transcriptional programs can clarify how PCP cues integrate with small GTPase and cytoskeletal dynamics.
Prickle4 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 PRICKLE4 upregulation across a broader range of human cell types.
Prickle4 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 PRICKLE4 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Prickle4 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native PRICKLE4 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.