ADHγ CRISPR/Cas9 KO Plasmid (h): sc-402261
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ADHγ 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 ADHγ 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 | |
ADHγ CRISPR/Cas9 KO Plasmid (h) | sc-402261 | 20 µg | $397.00 |
Overview
ADH1C encodes the human alcohol dehydrogenase gamma subunit (ADHγ), a zinc-dependent cytosolic oxidoreductase that catalyzes the NAD⁺-dependent oxidation of ethanol and other short-chain alcohols and aldehydes. This enzymatic activity supports alcohol and retinoid metabolism and intersects with cellular redox homeostasis by influencing the NADH/NAD⁺ balance and downstream aldehyde handling pathways. Variation or dysregulation in ADH1C-linked metabolic flux can modulate acetaldehyde burden and oxidative stress responses, processes implicated in liver injury, carcinogen metabolism, and broader metabolic phenotypes. As part of the ADH gene cluster, ADHγ is also relevant for studies of tissue-specific detoxification and xenobiotic processing in hepatic and upper aerodigestive tract biology.
ADHγ CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the ADH1C gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ADH1C 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 ADH1C 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 ADHγ protein expression.
This CRISPR knockout system enables efficient generation of ADH1C-deficient cell models for investigation of ADHγ signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting ADH1C exon(s) critical for ADHγ 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 ADH1C genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ADHγ CRISPR/Cas9 KO Plasmid (h) and ADHγ CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the ADH1C locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ADHγ HDR Plasmid (h) and ADHγ HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by ADH1C homology arms to support homology-directed repair at defined ADH1C 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.