ADH7 CRISPR/Cas9 KO Plasmid (m2): sc-419006-KO-2
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ADH7 CRISPR/Cas9 Knockout (KO) Plasmid (m2) 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 ADH7 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 | |
ADH7 CRISPR/Cas9 KO Plasmid (m2) | sc-419006-KO-2 | 20 µg | $397.00 |
Overview
Adh7 encodes alcohol dehydrogenase 7 (ADH7), an NAD-dependent oxidoreductase that contributes to the metabolism of retinoids and a range of alcohol and aldehyde substrates, thereby influencing cellular redox balance and detoxification capacity. In mouse tissues where it is expressed, ADH7 activity can intersect with retinol-to-retinal conversion steps that feed into retinoic acid signaling, a pathway central to differentiation programs and epithelial homeostasis. Altered aldehyde handling and retinoid metabolism are frequently linked to oxidative stress responses and dysregulated growth control, making Adh7 a useful node for studying metabolic contributions to tissue remodeling and disease-relevant phenotypes. Because alcohol/aldehyde metabolism also impacts lipid and inflammatory signaling, Adh7 perturbation can be leveraged to probe crosstalk between metabolic enzymes and transcriptional programs downstream of retinoid-regulated networks.
ADH7 CRISPR/Cas9 KO Plasmid (m2) is a pool of plasmids designed for targeted disruption of the Adh7 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Adh7 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 Adh7 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 ADH7 protein expression.
This CRISPR knockout system enables efficient generation of Adh7-deficient cell models for investigation of ADH7 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Adh7 exon(s) critical for ADH7 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 Adh7 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ADH7 CRISPR/Cas9 KO Plasmid (m) and ADH7 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Adh7 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ADH7 HDR Plasmid (m) and ADH7 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Adh7 homology arms to support homology-directed repair at defined Adh7 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.