VE-cadherin-2 CRISPR/Cas9 KO Plasmid (h): sc-401695
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- VE-cadherin-2 CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the VE-cadherin-2 genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: VE-cadherin-2 Antibody (F-4): sc-515467
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
VE-cadherin-2 CRISPR/Cas9 KO Plasmid (h) | sc-401695 | 20 µg | $397.00 |
Overview
PCDH12 encodes VE-cadherin-2, a calcium-dependent adhesion molecule enriched in vascular endothelial cells that supports stable cell–cell junctions and coordinated barrier formation. By engaging cadherin–catenin complexes and linking to the actin cytoskeleton, VE-cadherin-2 contributes to adherens junction organization, endothelial polarity, and regulation of permeability during angiogenic remodeling. Its activity intersects with signaling programs that tune junctional dynamics, including pathways influencing cytoskeletal tension and endothelial responses to inflammatory or mechanical cues. Dysregulation of endothelial adhesion and barrier control is relevant to vascular dysfunction phenotypes and provides a mechanistic entry point for studying microvascular integrity in disease-relevant models.
VE-cadherin-2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the PCDH12 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the PCDH12 together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the PCDH12 open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish VE-cadherin-2 protein expression.
This CRISPR knockout system enables efficient generation of PCDH12-deficient cell models for investigation of VE-cadherin-2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting PCDH12 exon(s) critical for VE-cadherin-2 function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple PCDH12 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by VE-cadherin-2 CRISPR/Cas9 KO Plasmid (h) and VE-cadherin-2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the PCDH12 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by VE-cadherin-2 HDR Plasmid (h) and VE-cadherin-2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by PCDH12 homology arms to support homology-directed repair at defined PCDH12 target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.