
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
plexin-D1 CRISPR Activation Plasmid (h) | sc-405134-ACT | 20 µg | $397.00 |
Human PLXND1 encodes plexin-D1, a single-pass transmembrane receptor that mediates semaphorin-dependent guidance cues to regulate cell migration, cytoskeletal remodeling, and directional patterning. Plexin-D1 signaling integrates with Rho family GTPases and associated actin dynamics to influence endothelial behavior, angiogenic sprouting, and tissue morphogenesis. PLXND1 activity is also linked to context-dependent changes in invasive motility and vascular remodeling programs that are frequently studied in cancer biology and inflammatory microenvironments. As a result, plexin-D1 is routinely examined as a node connecting guidance pathways with cell–cell communication and extracellular matrix interactions.
plexin-D1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PLXND1 expression without altering the underlying DNA sequence.
plexin-D1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PLXND1 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 PLXND1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous plexin-D1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PLXND1 locus and enabling the study of plexin-D1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of plexin-D1 pathway restoration in tumor cells with silenced or reduced PLXND1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.