KOR-1 Double Nickase Plasmid (h): sc-401354-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KOR-1 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
- KOR-1 Double Nickase Plasmid (h) and KOR-1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting OPRK1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: KOR-1 Antibody (D-8): sc-374479
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KOR-1 Double Nickase Plasmid (h) | sc-401354-NIC | 20 µg | $410.00 | |||
KOR-1 Double Nickase Plasmid (h2) | sc-401354-NIC-2 | 20 µg | $410.00 |
OPRK1 encodes the human kappa opioid receptor (KOR-1), a Gi/Go-coupled GPCR that modulates neuronal excitability and neurotransmitter release in response to endogenous dynorphins. KOR-1 signaling inhibits adenylyl cyclase, reduces cAMP/PKA activity, and engages MAPK cascades including ERK1/2 and p38, with downstream effects on ion channel function and synaptic plasticity. The receptor participates in reward, stress responsivity, pain processing, and neuroendocrine regulation, and altered OPRK1 signaling has been studied in neuropsychiatric and nociceptive phenotypes. In vitro, OPRK1 provides a tractable node to connect GPCR signaling dynamics with transcriptional programs and cellular adaptation in relevant neuronal and engineered cell models.
KOR-1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the OPRK1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within OPRK1. 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 OPRK1 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 OPRK1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.