AKR7A2 Double Nickase Plasmid (h): sc-403377-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AKR7A2 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
- AKR7A2 Double Nickase Plasmid (h) and AKR7A2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting AKR7A2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: AKR7A2 Antibody (Y02): sc-100503
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AKR7A2 Double Nickase Plasmid (h) | sc-403377-NIC | 20 µg | $410.00 | |||
AKR7A2 Double Nickase Plasmid (h2) | sc-403377-NIC-2 | 20 µg | $410.00 |
AKR7A2 encodes aldo-keto reductase family 7 member A2, a cytosolic NADPH-dependent oxidoreductase that catalyzes the reduction of reactive aldehydes and ketones generated during xenobiotic metabolism and lipid peroxidation. Through detoxification of electrophilic carbonyl species, AKR7A2 contributes to cellular redox homeostasis and protection from oxidative and carbonyl stress, intersecting with aldehyde metabolism and broader phase I/phase II metabolic networks. Altered handling of reactive aldehydes has been linked to tissue injury and inflammation, and variation in AKR7A2 activity is studied in contexts where metabolic stress and carcinogen processing influence cellular viability and genomic integrity. These properties make AKR7A2 a useful target for investigating mechanisms of detoxification, stress-adaptive signaling, and metabolism-associated disease phenotypes in human cell models.
AKR7A2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the AKR7A2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within AKR7A2. 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 AKR7A2 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 AKR7A2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.