βENaC CRISPR/Cas9 KO Plasmid (m): sc-422826
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- βENaC 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 βENaC 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: βENaC Antibody (D-3): sc-25354
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
βENaC CRISPR/Cas9 KO Plasmid (m) | sc-422826 | 20 µg | $397.00 |
Overview
Scnn1b encodes the mouse β subunit of the epithelial sodium channel (βENaC), a core component of amiloride-sensitive Na⁺ uptake across apical membranes of epithelial cells. Together with α and γ subunits, βENaC helps govern transepithelial sodium transport, airway surface liquid hydration, and epithelial barrier physiology. ENaC activity is tightly regulated by proteolytic activation, membrane trafficking, and ubiquitin-dependent turnover via the NEDD4L pathway, linking Scnn1b to ion homeostasis and epithelial stress responses. Altered ENaC function is widely studied in models of airway mucus obstruction and impaired mucociliary clearance, as well as renal sodium handling and blood pressure regulation.
βENaC CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Scnn1b gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Scnn1b 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 Scnn1b 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 βENaC protein expression.
This CRISPR knockout system enables efficient generation of Scnn1b-deficient cell models for investigation of βENaC signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Scnn1b exon(s) critical for βENaC 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 Scnn1b genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by βENaC CRISPR/Cas9 KO Plasmid (m) and βENaC CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Scnn1b locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by βENaC HDR Plasmid (m) and βENaC HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Scnn1b homology arms to support homology-directed repair at defined Scnn1b 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.