ADH5 Double Nickase Plasmid (h): sc-403859-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ADH5 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
- ADH5 Double Nickase Plasmid (h) and ADH5 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ADH5. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ADH5 Antibody (B-1): sc-518202
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ADH5 Double Nickase Plasmid (h) | sc-403859-NIC | 20 µg | $410.00 | |||
ADH5 Double Nickase Plasmid (h2) | sc-403859-NIC-2 | 20 µg | $410.00 |
ADH5 (alcohol dehydrogenase 5), also known as S-nitrosoglutathione reductase, is a cytosolic dehydrogenase that catalyzes the NADH-dependent reduction of S-nitrosoglutathione and related aldehyde substrates. Through control of protein S-nitrosylation and nitric oxide bioavailability, ADH5 influences redox homeostasis, antioxidant responses, and nitrosative stress signaling. This activity interfaces with glutathione metabolism and detoxification pathways that modulate inflammatory signaling and cellular resilience to oxidative damage. Altered ADH5 function has been associated with dysregulated nitrosative stress and has been explored in disease-relevant contexts including cancer biology, cardiovascular and pulmonary inflammation, and neurodegenerative processes.
ADH5 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ADH5 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ADH5. 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 ADH5 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 ADH5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.