αENaC CRISPR/Cas9 KO Plasmid (m): sc-422825
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- αENaC 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 αENaC 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 | |
αENaC CRISPR/Cas9 KO Plasmid (m) | sc-422825 | 20 µg | $397.00 |
Overview
Scnn1a encodes the alpha subunit of the epithelial sodium channel (αENaC), a rate-limiting component of amiloride-sensitive Na⁺ absorption across apical membranes in airway, kidney, and other epithelia. αENaC assembles with β and γ subunits to control transepithelial sodium transport, thereby influencing airway surface liquid homeostasis and renal sodium balance. Channel activity is regulated through proteolytic activation and ubiquitin-dependent turnover, prominently involving Nedd4-2-mediated endocytosis and hormonal cues that tune sodium handling. Dysregulation of ENaC-dependent ion transport is widely used as a mechanistic framework for studying epithelial fluid imbalance, mucus dehydration, and salt-sensitive physiology in mouse models.
αENaC CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Scnn1a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Scnn1a 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 Scnn1a 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 αENaC protein expression.
This CRISPR knockout system enables efficient generation of Scnn1a-deficient cell models for investigation of αENaC signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Scnn1a exon(s) critical for αENaC 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 Scnn1a genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by αENaC CRISPR/Cas9 KO Plasmid (m) and αENaC CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Scnn1a locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by αENaC HDR Plasmid (m) and αENaC HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Scnn1a homology arms to support homology-directed repair at defined Scnn1a 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.