OB-cadherin CRISPR Activation Plasmid (h): sc-401051-ACT

CDH11 encodes OB-cadherin, a classical cadherin that mediates Ca²⁺-dependent homophilic cell–cell adhesion and supports tissue morphogenesis, mesenchymal cohesion, and stromal organization. OB-cadherin engagement links to catenins and the actin cytoskeleton, influencing junctional stability, mechanotransduction, and contact-dependent signaling that intersects with pathways such as Wnt/β-catenin and Rho GTPase–regulated cytoskeletal dynamics. In human biology, CDH11 is prominently associated with fibroblast and osteoblast lineage programs and contributes to extracellular matrix remodeling and migratory phenotypes. Dysregulated CDH11 expression has been reported in contexts including fibrosis, arthritis-related stromal activation, and tumor–stroma interactions, making it relevant for studies of adhesion-dependent signaling and microenvironmental regulation.

OB-cadherin CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CDH11 expression without altering the underlying DNA sequence.

OB-cadherin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CDH11 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 CDH11 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous OB-cadherin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CDH11 locus and enabling the study of OB-cadherin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of OB-cadherin pathway restoration in tumor cells with silenced or reduced CDH11 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.