
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Ninjurin-1 CRISPR Activation Plasmid (h) | sc-403990-ACT | 20 µg | $397.00 |
NINJ1 encodes Ninjurin-1, a transmembrane adhesion protein induced by nerve injury and broadly expressed in immune and parenchymal tissues. Ninjurin-1 contributes to cell–cell and cell–matrix interactions, regulating leukocyte trafficking, endothelial activation, and inflammatory signaling programs. It has been linked to macrophage-mediated responses and innate immune pathways that shape tissue damage and repair, with reported relevance to neuroinflammation and vascular inflammatory conditions. Altered NINJ1 expression has been observed in disease-associated contexts where adhesion dynamics and inflammatory cell recruitment influence pathology.
Ninjurin-1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous NINJ1 expression without altering the underlying DNA sequence.
Ninjurin-1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the NINJ1 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 NINJ1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Ninjurin-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native NINJ1 locus and enabling the study of Ninjurin-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Ninjurin-1 pathway restoration in tumor cells with silenced or reduced NINJ1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.