ADHβ Double Nickase Plasmid (h): sc-402141-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ADHβ 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
- ADHβ Double Nickase Plasmid (h) and ADHβ Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ADH1B. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ADHβ Double Nickase Plasmid (h) | sc-402141-NIC | 20 µg | $410.00 | |||
ADHβ Double Nickase Plasmid (h2) | sc-402141-NIC-2 | 20 µg | $410.00 |
ADH1B encodes the human alcohol dehydrogenase beta subunit (ADHβ), a cytosolic zinc-dependent oxidoreductase that catalyzes the NAD⁺-dependent conversion of ethanol and other short-chain alcohols to their corresponding aldehydes. This enzymatic activity integrates with aldehyde detoxification and broader cellular redox homeostasis by influencing NADH/NAD⁺ balance, thereby intersecting with oxidative stress responses and intermediary metabolism. Genetic and functional variation in ADH1B is widely studied for its impact on ethanol metabolism kinetics and acetaldehyde burden, which can modulate susceptibility to alcohol-related pathophysiology and associated tissue injury. ADH1B also serves as a metabolic node relevant to pharmacogenomic and toxicology research involving xenobiotic alcohol substrates.
ADHβ Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ADH1B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ADH1B. 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 ADH1B 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 ADH1B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.