DD1 Double Nickase Plasmid (h): sc-403693-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DD1 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
- DD1 Double Nickase Plasmid (h) and DD1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting AKR1C1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DD1 Double Nickase Plasmid (h) | sc-403693-NIC | 20 µg | $410.00 | |||
DD1 Double Nickase Plasmid (h2) | sc-403693-NIC-2 | 20 µg | $410.00 |
AKR1C1 encodes aldo-keto reductase family 1 member C1 (DD1), an NADPH-dependent oxidoreductase that interconverts reactive aldehydes and ketosteroids, including progesterone-derived and androgen/estrogen precursors. By regulating local steroid metabolism and detoxifying lipid peroxidation products, DD1 influences redox homeostasis, xenobiotic processing, and hormone-responsive transcriptional programs. Altered AKR1C1 activity has been associated with shifts in steroid signaling and oxidative stress responses that are frequently studied in endocrine biology and cancer-related pathways. As a cytosolic enzyme at the interface of metabolism and signaling, AKR1C1 is commonly interrogated for its impact on cell proliferation, differentiation, and stress adaptation.
DD1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the AKR1C1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within AKR1C1. 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 AKR1C1 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 AKR1C1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.