γENaC CRISPR/Cas9 KO Plasmid (m): sc-422827
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- γENaC CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 γENaC 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
γENaC CRISPR/Cas9 KO Plasmid (m) | sc-422827 | 20 µg | $397.00 |
Overview
Scnn1g encodes the γ subunit of the epithelial sodium channel (γENaC), a key determinant of amiloride-sensitive Na⁺ entry across apical membranes in epithelial tissues. Together with α and β subunits, γENaC regulates transepithelial sodium transport that influences airway surface liquid homeostasis, renal sodium reabsorption, and fluid volume balance. Channel activity is controlled by proteolytic processing and membrane trafficking, integrating with aldosterone-responsive programs and downstream ion transport networks such as Na⁺/K⁺-ATPase–coupled salt handling. Dysregulation of ENaC subunits has been linked to altered epithelial hydration and salt balance phenotypes, supporting its relevance in studies of airway and kidney physiology and related ion transport disorders.
γENaC CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Scnn1g gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Scnn1g 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 Scnn1g 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 γENaC protein expression.
This CRISPR knockout system enables efficient generation of Scnn1g-deficient cell models for investigation of γENaC signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Scnn1g exon(s) critical for γENaC 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 Scnn1g genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by γENaC CRISPR/Cas9 KO Plasmid (m) and γENaC CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Scnn1g locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by γENaC HDR Plasmid (m) and γENaC HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Scnn1g homology arms to support homology-directed repair at defined Scnn1g 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.