PCDHGA11 CRISPR Activation Plasmid (h): sc-407326-ACT

PCDHGA11 encodes protocadherin gamma-A11, a calcium-dependent cell-adhesion protein in the clustered protocadherin family that contributes to cell–cell recognition and tissue architecture. Protocadherins support contact-dependent signaling, membrane organization, and cytoskeletal dynamics that influence neuronal connectivity and broader epithelial or immune cell interactions. Altered protocadherin expression patterns are frequently linked to dysregulated adhesion and lineage programs observed in neurodevelopmental phenotypes and cancer-related processes. As part of adhesion and surface receptor networks, PCDHGA11 is studied for its impact on cell identity, synaptic or junctional organization, and transcriptional states downstream of intercellular contact.

PCDHGA11 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PCDHGA11 expression without altering the underlying DNA sequence.

PCDHGA11 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PCDHGA11 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 PCDHGA11 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PCDHGA11 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PCDHGA11 locus and enabling the study of PCDHGA11-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PCDHGA11 pathway restoration in tumor cells with silenced or reduced PCDHGA11 expression.

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