ADH7 Double Nickase Plasmid (h): sc-405066-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ADH7 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
- ADH7 Double Nickase Plasmid (h) and ADH7 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ADH7. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ADH7 Double Nickase Plasmid (h) | sc-405066-NIC | 20 µg | $410.00 | |||
ADH7 Double Nickase Plasmid (h2) | sc-405066-NIC-2 | 20 µg | $410.00 |
ADH7 encodes alcohol dehydrogenase 7 (class IV), a cytosolic NAD(P)+-dependent oxidoreductase that catalyzes oxidation of ethanol and diverse retinoid- and lipid-derived alcohols, contributing to aldehyde generation and downstream metabolism. It is prominently expressed in upper gastrointestinal epithelia where it interfaces with retinoid homeostasis, redox balance, and detoxification of reactive carbonyl species. Through its role in ethanol/retinol metabolism and aldehyde handling, ADH7 is relevant to pathways influencing epithelial differentiation, oxidative stress responses, and barrier biology. Altered ADH7 activity or expression has been investigated in the context of interindividual variation in alcohol-related aldehyde burden and susceptibility to epithelial injury and carcinogenesis.
ADH7 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ADH7 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ADH7. 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 ADH7 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 ADH7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.