NMDAε3 Double Nickase Plasmid (h): sc-402942-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NMDAε3 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
- NMDAε3 Double Nickase Plasmid (h) and NMDAε3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GRIN2C. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NMDAε3 Double Nickase Plasmid (h) | sc-402942-NIC | 20 µg | $410.00 | |||
NMDAε3 Double Nickase Plasmid (h2) | sc-402942-NIC-2 | 20 µg | $410.00 |
GRIN2C encodes the NMDA receptor subunit NMDAε3 (GluN2C), a glutamate-gated ion channel component that assembles with NR1 and other NR2 subunits to regulate excitatory synaptic transmission. NMDAε3 contributes to receptor biophysical properties that shape calcium influx, synaptic plasticity, and activity-dependent gene expression, linking it to core neurodevelopmental and synaptic signaling pathways. Through coupling to downstream Ca2+-dependent cascades such as CaMK and CREB-related transcriptional programs, GRIN2C influences neuronal network maturation and circuit function. Altered NMDA receptor subunit composition and GRIN2C dysregulation have been studied in the context of neuropsychiatric and neurodevelopmental phenotypes, supporting its relevance for mechanistic studies of excitatory neurotransmission.
NMDAε3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GRIN2C locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GRIN2C. 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 GRIN2C 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 GRIN2C-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.