KA2 Double Nickase Plasmid (h): sc-405272-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KA2 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
- KA2 Double Nickase Plasmid (h) and KA2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GRIK5. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KA2 Double Nickase Plasmid (h) | sc-405272-NIC | 20 µg | $410.00 | |||
KA2 Double Nickase Plasmid (h2) | sc-405272-NIC-2 | 20 µg | $410.00 |
GRIK5 encodes the kainate receptor subunit KA2, an ionotropic glutamate receptor component that assembles with other kainate subunits to shape excitatory synaptic transmission and neuronal network excitability. KA2 contributes to ligand-gated cation channel function, influencing synaptic plasticity, presynaptic modulation, and downstream calcium- and MAPK-linked signaling pathways. Altered glutamatergic signaling involving GRIK5 has been investigated in neurodevelopmental and neuropsychiatric contexts, including seizure susceptibility and circuit dysfunction, where receptor composition can affect excitatory–inhibitory balance. As a synaptic membrane protein, KA2 is also relevant to studies of receptor trafficking, synapse maturation, and activity-dependent remodeling in human neuronal models.
KA2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GRIK5 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GRIK5. 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 GRIK5 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 GRIK5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.