DHRS2 Double Nickase Plasmid (h): sc-404988-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DHRS2 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
- DHRS2 Double Nickase Plasmid (h) and DHRS2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DHRS2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: DHRS2 Antibody (1F10): sc-517054
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DHRS2 Double Nickase Plasmid (h) | sc-404988-NIC | 20 µg | $410.00 | |||
DHRS2 Double Nickase Plasmid (h2) | sc-404988-NIC-2 | 20 µg | $410.00 |
Human DHRS2 (dehydrogenase/reductase 2) encodes an NADPH-dependent oxidoreductase of the short-chain dehydrogenase/reductase superfamily that supports cellular redox homeostasis and metabolism. DHRS2 has been linked to regulation of stress responses and cell-cycle control, including reported interactions with p53-associated signaling and pathways that influence proliferation and senescence. By modulating intracellular redox balance, DHRS2 can affect oxidative stress handling and downstream transcriptional programs relevant to genome stability. Altered DHRS2 expression has been observed across multiple disease contexts, making it a useful target for mechanistic studies of metabolic reprogramming and stress-adaptive signaling in human cells.
DHRS2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DHRS2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DHRS2. 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 DHRS2 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 DHRS2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.