NRK Double Nickase Plasmid (m): sc-424201-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NRK Double Nickase Plasmid (m) 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
- NRK Double Nickase Plasmid (m) and NRK Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Nrk. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NRK Double Nickase Plasmid (m) | sc-424201-NIC | 20 µg | $410.00 | |||
NRK Double Nickase Plasmid (m2) | sc-424201-NIC-2 | 20 µg | $410.00 |
Mouse Nrk encodes Nik-related kinase (NRK), a serine/threonine protein kinase implicated in signaling networks that coordinate cell proliferation, stress responses, and tissue development. NRK has been linked to regulation of kinase cascades, including MAPK-associated processes, and contributes to control of cellular growth and differentiation programs. In mice, Nrk function is particularly relevant to placental development and trophoblast biology, making it useful for studying developmental regulation and maternal–fetal interface signaling. Dysregulated kinase signaling involving NRK has been investigated in contexts of abnormal growth and cancer-related pathways, supporting its relevance for mechanistic disease modeling in biomedical research.
NRK Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Nrk locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Nrk. 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 Nrk 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 Nrk-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.