KCNQ3 Double Nickase Plasmid (h): sc-403544-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KCNQ3 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
- KCNQ3 Double Nickase Plasmid (h) and KCNQ3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KCNQ3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KCNQ3 Double Nickase Plasmid (h) | sc-403544-NIC | 20 µg | $410.00 | |||
KCNQ3 Double Nickase Plasmid (h2) | sc-403544-NIC-2 | 20 µg | $410.00 |
KCNQ3 encodes the Kv7.3 voltage-gated potassium channel subunit that assembles with other Kv7 family members, particularly Kv7.2, to form M-type K⁺ currents that stabilize resting membrane potential and limit repetitive firing. By shaping subthreshold excitability and action potential adaptation, KCNQ3 contributes to neuronal network oscillations and synaptic integration across central and peripheral nervous systems. Channel activity is modulated by phosphatidylinositol 4,5-bisphosphate (PIP2) and Gq/PLC-coupled signaling, linking KCNQ3 function to receptor-driven control of membrane excitability. Genetic and functional perturbation of KCNQ3 has been associated with neurodevelopmental and seizure-related phenotypes, making it a useful target for mechanistic studies of ion channel regulation and excitability-dependent signaling.
KCNQ3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KCNQ3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KCNQ3. 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 KCNQ3 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 KCNQ3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.