
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LYPD2 CRISPR Activation Plasmid (h) | sc-408607-ACT | 20 µg | $397.00 |
LYPD2 (Ly6/PLAUR domain containing 2) encodes a GPI-anchored, Ly6/uPAR family cell-surface protein implicated in modulating extracellular ligand interactions and membrane-proximal signaling. As a member of the Ly6 superfamily, LYPD2 is linked to processes that shape cell adhesion, receptor organization, and context-dependent signal transduction at the plasma membrane. Expression patterns in epithelial and neuronal-associated tissues suggest roles in differentiation and tissue homeostasis, with dysregulation reported in molecular profiling studies of cancer and other complex diseases. These features make LYPD2 relevant for investigating cell-state regulation, surface-protein networks, and pathway remodeling in disease models.
LYPD2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous LYPD2 expression without altering the underlying DNA sequence.
LYPD2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the LYPD2 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 LYPD2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous LYPD2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native LYPD2 locus and enabling the study of LYPD2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of LYPD2 pathway restoration in tumor cells with silenced or reduced LYPD2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.