TASK-1 Double Nickase Plasmid (h): sc-403477-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TASK-1 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
- TASK-1 Double Nickase Plasmid (h) and TASK-1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KCNK3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TASK-1 Double Nickase Plasmid (h) | sc-403477-NIC | 20 µg | $410.00 | |||
TASK-1 Double Nickase Plasmid (h2) | sc-403477-NIC-2 | 20 µg | $410.00 |
KCNK3 encodes TASK-1 (K2P3.1), a two-pore domain potassium channel that generates background K⁺ leak currents to stabilize resting membrane potential and tune cellular excitability. TASK-1 activity is regulated by extracellular pH, lipid signaling, and GPCR-linked pathways that modulate membrane conductance and downstream Ca²⁺-dependent signaling. In human tissues, TASK-1 contributes to electrophysiological control in cardiac and pulmonary vascular cells as well as neurons, influencing processes such as action potential repolarization, vascular tone regulation, and stimulus–secretion coupling. Dysregulated KCNK3/TASK-1 function has been associated with altered cardiopulmonary and neurophysiological phenotypes, making it a useful target for mechanistic studies of ion channel–dependent signaling networks.
TASK-1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KCNK3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KCNK3. 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 KCNK3 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 KCNK3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.