ADHγ Double Nickase Plasmid (h): sc-402261-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ADHγ Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- ADHγ Double Nickase Plasmid (h) and ADHγ Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ADH1C. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ADHγ Double Nickase Plasmid (h) | sc-402261-NIC | 20 µg | $410.00 | |||
ADHγ Double Nickase Plasmid (h2) | sc-402261-NIC-2 | 20 µg | $410.00 |
ADH1C encodes human alcohol dehydrogenase gamma (ADHγ), a cytosolic zinc-dependent oxidoreductase that catalyzes the NAD⁺-dependent oxidation of ethanol and other aliphatic alcohols to their corresponding aldehydes. As part of the ADH gene cluster, ADHγ contributes to hepatic and gastrointestinal xenobiotic metabolism and influences cellular redox balance through NADH production. Variation or altered regulation of ADH1C can modulate acetaldehyde exposure and downstream oxidative stress and aldehyde detoxification pathways, linking this enzyme to susceptibility phenotypes in alcohol-related tissue injury and broader metabolic dysregulation. ADH1C is also used as a functional marker in studies of hepatocyte differentiation, liver metabolism, and enzyme kinetics across ADH isoforms.
ADHγ Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ADH1C locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ADH1C. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt ADH1C function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of ADH1C-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.