ADH1 Double Nickase Plasmid (h): sc-402260-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ADH1 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
- ADH1 Double Nickase Plasmid (h) and ADH1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ADH1A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ADH1 Double Nickase Plasmid (h) | sc-402260-NIC | 20 µg | $410.00 | |||
ADH1 Double Nickase Plasmid (h2) | sc-402260-NIC-2 | 20 µg | $410.00 |
Human ADH1A encodes alcohol dehydrogenase 1A (ADH1), a cytosolic zinc-dependent oxidoreductase that catalyzes NAD⁺-dependent oxidation of ethanol and other short-chain aliphatic and aromatic alcohols to their corresponding aldehydes. This activity contributes to hepatic alcohol and retinoid metabolism, influencing redox balance and metabolite flux that can impact oxidative stress responses and lipid handling pathways. Variation or dysregulation in alcohol dehydrogenase activity is studied in the context of ethanol-related tissue injury and metabolic phenotypes, and ADH1A expression is frequently used as a marker of hepatocyte differentiation state in experimental systems. ADH1A/ADH1 also provides a tractable node for dissecting aldehyde handling and downstream signaling linked to cellular stress and inflammatory programs.
ADH1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ADH1A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ADH1A. 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 ADH1A 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 ADH1A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.