SK1 Double Nickase Plasmid (h): sc-403325-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SK1 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
- SK1 Double Nickase Plasmid (h) and SK1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KCNN1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SK1 Double Nickase Plasmid (h) | sc-403325-NIC | 20 µg | $410.00 | |||
SK1 Double Nickase Plasmid (h2) | sc-403325-NIC-2 | 20 µg | $410.00 |
Human KCNN1 encodes the small-conductance Ca2+-activated potassium channel SK1, a calmodulin-gated K+ conductance that links intracellular Ca2+ dynamics to membrane repolarization. By shaping afterhyperpolarization and firing patterns, SK1 contributes to Ca2+-dependent control of neuronal excitability and signal integration, with additional roles reported in other electrically active and secretory cell types. KCNN1 activity intersects with Ca2+/calmodulin signaling, excitability-dependent transcriptional programs, and ion homeostasis pathways that influence cellular stress responses. Dysregulated SK-family channel function has been studied in the context of neurophysiology and neuropsychiatric phenotypes, where altered intrinsic excitability and network synchronization are relevant experimental readouts.
SK1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KCNN1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KCNN1. 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 KCNN1 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 KCNN1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.