KA1 Double Nickase Plasmid (h): sc-403522-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KA1 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
- KA1 Double Nickase Plasmid (h) and KA1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GRIK4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KA1 Double Nickase Plasmid (h) | sc-403522-NIC | 20 µg | $410.00 | |||
KA1 Double Nickase Plasmid (h2) | sc-403522-NIC-2 | 20 µg | $410.00 |
GRIK4 encodes the kainate-type ionotropic glutamate receptor subunit KA1, a component of excitatory neurotransmission that modulates synaptic signaling and neuronal network excitability. KA1 contributes to receptor assembly and gating properties within glutamatergic synapses, supporting activity-dependent plasticity and circuit-level information processing. Through coupling of glutamate receptor activity to calcium-permeable signaling cascades, GRIK4 influences downstream pathways involved in synaptic remodeling and neuronal survival. Genetic and expression studies have linked GRIK4/KA1 dysregulation to neuropsychiatric and neurodevelopmental phenotypes, supporting its relevance for mechanistic research in CNS disease models.
KA1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GRIK4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GRIK4. 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 GRIK4 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 GRIK4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.