
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
cadherin-26 CRISPR Activation Plasmid (m) | sc-436285-ACT | 20 µg | $397.00 | |||
cadherin-26 CRISPR Activation Plasmid (m2) | sc-436285-ACT-2 | 20 µg | $397.00 |
Mouse Cdh26 encodes cadherin-26, a calcium-dependent cell–cell adhesion molecule within the cadherin superfamily that contributes to epithelial tissue organization and maintenance of barrier integrity. Through adherens junction–associated interactions, cadherin-26 supports cell polarity, contact-dependent signaling, and coordinated regulation of cytoskeletal dynamics that influence epithelial differentiation and remodeling. Altered cadherin expression patterns are frequently linked to changes in adhesion, migration, and inflammatory tissue responses, making Cdh26 a useful target for studying epithelial homeostasis and context-dependent remodeling programs. In mouse systems, Cdh26 modulation can help interrogate how adhesion networks intersect with developmental and immune-associated signaling pathways in barrier tissues.
cadherin-26 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Cdh26 expression without altering the underlying DNA sequence.
cadherin-26 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Cdh26 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 Cdh26 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous cadherin-26 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Cdh26 locus and enabling the study of cadherin-26-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of cadherin-26 pathway restoration in tumor cells with silenced or reduced Cdh26 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.