
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
T2-cadherin CRISPR Activation Plasmid (h) | sc-401926-ACT | 20 µg | $397.00 |
CDH10 encodes T2-cadherin, a calcium-dependent cell–cell adhesion molecule of the cadherin superfamily that contributes to tissue architecture by supporting homophilic interactions at the plasma membrane. Through coupling of adhesion complexes to actin cytoskeleton remodeling, T2-cadherin influences contact-mediated signaling, cell polarity, and coordinated migration programs. CDH10 expression is prominent in neuronal and epithelial contexts, linking it to pathways that shape neurite outgrowth and synaptic connectivity as well as epithelial organization. Dysregulated cadherin-mediated adhesion, including altered CDH10 activity, is frequently examined in studies of developmental abnormalities and tumor biology where changes in cell adhesion and invasiveness are key phenotypes.
T2-cadherin CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CDH10 expression without altering the underlying DNA sequence.
T2-cadherin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CDH10 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 CDH10 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous T2-cadherin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CDH10 locus and enabling the study of T2-cadherin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of T2-cadherin pathway restoration in tumor cells with silenced or reduced CDH10 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.