
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Dpl CRISPR Activation Plasmid (h) | sc-403482-ACT | 20 µg | $397.00 |
PRND encodes the human Doppel protein (Dpl), a glycosylphosphatidylinositol-anchored cell-surface glycoprotein structurally related to prion protein and enriched in reproductive tissues. Dpl participates in processes linked to membrane microdomains, protein quality control, and cellular stress responses, with reported connections to redox balance and apoptotic signaling depending on cellular context. Altered PRND expression has been investigated in relation to neurodegenerative prion biology and tumor-associated phenotypes, supporting its use as a marker for pathway interrogation rather than direct causality. Modulating Dpl levels enables mechanistic studies of cell survival, differentiation states, and prion-related protein networks in relevant human models.
Dpl CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PRND expression without altering the underlying DNA sequence.
Dpl CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PRND locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the PRND transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Dpl expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PRND locus and enabling the study of Dpl-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Dpl pathway restoration in tumor cells with silenced or reduced PRND expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.