NCX3 Double Nickase Plasmid (m): sc-431066-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NCX3 Double Nickase Plasmid (m) 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
- NCX3 Double Nickase Plasmid (m) and NCX3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Slc8a3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NCX3 Double Nickase Plasmid (m) | sc-431066-NIC | 20 µg | $410.00 | |||
NCX3 Double Nickase Plasmid (m2) | sc-431066-NIC-2 | 20 µg | $410.00 |
Slc8a3 encodes the mouse Na⁺/Ca²⁺ exchanger NCX3, a plasma membrane transporter that helps maintain intracellular Ca²⁺ homeostasis by coupling Ca²⁺ efflux (or influx under specific electrochemical conditions) to Na⁺ gradients. By shaping cytosolic Ca²⁺ dynamics, NCX3 influences excitation–contraction coupling, synaptic signaling, and mitochondrial Ca²⁺ handling, thereby integrating with broader calcium signaling networks that regulate metabolism, membrane excitability, and stress responses. NCX3 activity is particularly relevant in excitable tissues where rapid Ca²⁺ clearance is required, including neurons and muscle. Dysregulated Na⁺/Ca²⁺ exchange and Ca²⁺ overload pathways have been linked to mechanisms of neurodegeneration, ischemic injury responses, and myopathy-associated cellular dysfunction, making Slc8a3 a useful target for mechanistic studies.
NCX3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Slc8a3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Slc8a3. 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 Slc8a3 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 Slc8a3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.