KIR3.4 Double Nickase Plasmid (h): sc-404643-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KIR3.4 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
- KIR3.4 Double Nickase Plasmid (h) and KIR3.4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KCNJ5. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: KIR3.4 Antibody (8D2): sc-293378
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KIR3.4 Double Nickase Plasmid (h) | sc-404643-NIC | 20 µg | $410.00 | |||
KIR3.4 Double Nickase Plasmid (h2) | sc-404643-NIC-2 | 20 µg | $410.00 |
Human KCNJ5 encodes the inwardly rectifying potassium channel subunit KIR3.4 (GIRK4), which assembles with other GIRK family members to form G protein–gated K+ channels that couple GPCR signaling to membrane hyperpolarization. By conducting potassium under the control of Gβγ subunits, KIR3.4 helps regulate cellular excitability, pacemaking activity, and stimulus-dependent changes in membrane potential that shape calcium entry and downstream signaling. KCNJ5 is implicated in aldosterone regulation in adrenal zona glomerulosa cells, and recurrent variants have been associated with disorders of mineralocorticoid excess and related cardiometabolic phenotypes. Altered KIR3.4 function is also relevant to electrophysiology-focused studies of cardiac and neuroendocrine signaling, including GPCR pathway modulation and ion homeostasis.
KIR3.4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KCNJ5 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KCNJ5. 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 KCNJ5 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 KCNJ5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.