CD155 CRISPR Activation Plasmid (m): sc-424585-ACT

Mouse Pvr encodes CD155, an immunoglobulin superfamily adhesion molecule that functions as a ligand for DNAM-1 (CD226) as well as inhibitory receptors such as TIGIT and CD96, shaping immune synapse formation and cytotoxic lymphocyte activity. CD155 also supports cell adhesion and motility through interactions with extracellular matrix and cytoskeletal regulators, linking to processes that influence tissue remodeling and inflammation. In the nervous system it is known as a poliovirus receptor homolog and contributes to cell–cell contact dynamics. Dysregulated CD155 expression is frequently studied in the context of tumor immunology, viral interactions, and immune evasion mechanisms, making Pvr a useful node for investigating immunoreceptor signaling and microenvironmental regulation in mouse models.

CD155 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Pvr expression without altering the underlying DNA sequence.

CD155 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Pvr 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 Pvr transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CD155 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Pvr locus and enabling the study of CD155-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CD155 pathway restoration in tumor cells with silenced or reduced Pvr expression.

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