KCNE1 Double Nickase Plasmid (h): sc-404317-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KCNE1 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
- KCNE1 Double Nickase Plasmid (h) and KCNE1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KCNE1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KCNE1 Double Nickase Plasmid (h) | sc-404317-NIC | 20 µg | $410.00 | |||
KCNE1 Double Nickase Plasmid (h2) | sc-404317-NIC-2 | 20 µg | $410.00 |
KCNE1 encodes a single-pass transmembrane β-subunit that modulates voltage-gated potassium channel function, most prominently the KCNQ1/Kv7.1 complex that carries the slow delayed rectifier current (IKs). By tuning channel gating kinetics, membrane trafficking, and pharmacologic sensitivity, KCNE1 helps regulate cardiac repolarization and cellular excitability. This activity links KCNE1 to electrophysiological pathways controlling action potential duration and ion homeostasis in cardiomyocytes and other excitable tissues. Genetic variation or dysregulated expression of KCNE1 has been associated with inherited arrhythmia susceptibility and auditory phenotypes through effects on potassium flux in the heart and inner ear.
KCNE1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KCNE1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KCNE1. 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 KCNE1 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 KCNE1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.