μ-protocadherin CRISPR/Cas9 KO Plasmid (h): sc-406015
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- μ-protocadherin 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 μ-protocadherin 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: µ-protocadherin Antibody (A-11): sc-166953
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
μ-protocadherin CRISPR/Cas9 KO Plasmid (h) | sc-406015 | 20 µg | $397.00 |
Overview
CDHR5 encodes μ-protocadherin, a calcium-dependent cell–cell adhesion molecule enriched in epithelial tissues, where it contributes to apical junction organization, polarity maintenance, and barrier integrity. Through homophilic interactions and linkage to cytoskeletal and junctional complexes, μ-protocadherin helps coordinate epithelial morphogenesis and contact-dependent signaling that influences differentiation and tissue architecture. Altered CDHR5 expression has been associated with epithelial remodeling and dysregulated adhesion programs observed in gastrointestinal and other epithelial pathologies. As a surface adhesion receptor, CDHR5 is frequently examined in studies of junctional stability, epithelial plasticity, and microenvironment-dependent phenotypes.
μ-protocadherin CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CDHR5 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CDHR5 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 CDHR5 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 μ-protocadherin protein expression.
This CRISPR knockout system enables efficient generation of CDHR5-deficient cell models for investigation of μ-protocadherin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting CDHR5 exon(s) critical for μ-protocadherin 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 CDHR5 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by μ-protocadherin CRISPR/Cas9 KO Plasmid (h) and μ-protocadherin CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CDHR5 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by μ-protocadherin HDR Plasmid (h) and μ-protocadherin HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CDHR5 homology arms to support homology-directed repair at defined CDHR5 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.