CNOX CRISPR/Cas9 KO Plasmid (h): sc-412433
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CNOX 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 CNOX 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 | |
CNOX CRISPR/Cas9 KO Plasmid (h) | sc-412433 | 20 µg | $397.00 |
Overview
ENOX1 encodes the ecto-NOX disulfide–thiol exchanger CNOX, a plasma membrane–associated oxidoreductase that couples protein disulfide interchange with NADH oxidation and contributes to cell-surface redox homeostasis. ENOX1 activity has been linked to regulation of extracellular electron transfer, modulation of reactive oxygen species balance, and coordination of growth-related oscillatory redox processes that can influence proliferation and metabolic adaptation. Through its roles in redox signaling and membrane-associated electron transport, ENOX1 is studied in contexts of oxidative stress responses, vascular biology, and cellular phenotypes associated with altered redox control. Dysregulated ENOX1 expression or activity has been reported in multiple disease-associated transcriptional programs, supporting its utility as a mechanistic node for investigating redox-dependent signaling and metabolic reprogramming in human cells.
CNOX CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the ENOX1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ENOX1 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 ENOX1 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 CNOX protein expression.
This CRISPR knockout system enables efficient generation of ENOX1-deficient cell models for investigation of CNOX signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting ENOX1 exon(s) critical for CNOX 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 ENOX1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CNOX CRISPR/Cas9 KO Plasmid (h) and CNOX CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the ENOX1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CNOX HDR Plasmid (h) and CNOX HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by ENOX1 homology arms to support homology-directed repair at defined ENOX1 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.