KIR3.2 Double Nickase Plasmid (h): sc-405031-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KIR3.2 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
- KIR3.2 Double Nickase Plasmid (h) and KIR3.2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KCNJ6. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KIR3.2 Double Nickase Plasmid (h) | sc-405031-NIC | 20 µg | $410.00 | |||
KIR3.2 Double Nickase Plasmid (h2) | sc-405031-NIC-2 | 20 µg | $410.00 |
KCNJ6 encodes the human inwardly rectifying potassium channel KIR3.2 (GIRK2), a G protein–gated ion channel that couples GPCR signaling to membrane hyperpolarization and reduced cellular excitability. KIR3.2 contributes to potassium conductance in neurons and other excitable tissues, integrating neurotransmitter and neuromodulator inputs through Gβγ-mediated gating and shaping firing patterns, synaptic transmission, and network activity. This channel participates in pathways linking GPCR activation to ion homeostasis and electrophysiological control, with downstream effects on calcium entry and activity-dependent signaling. Dysregulation or genetic variation in KCNJ6 has been associated with neurophysiological and neurodevelopmental phenotypes, supporting its relevance in studies of excitability-driven disease mechanisms.
KIR3.2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KCNJ6 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KCNJ6. 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 KCNJ6 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 KCNJ6-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.