PMCA2 Double Nickase Plasmid (h): sc-403416-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PMCA2 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
- PMCA2 Double Nickase Plasmid (h) and PMCA2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ATP2B2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PMCA2 Double Nickase Plasmid (h) | sc-403416-NIC | 20 µg | $410.00 | |||
PMCA2 Double Nickase Plasmid (h2) | sc-403416-NIC-2 | 20 µg | $410.00 |
ATP2B2 encodes plasma membrane Ca2+-transporting ATPase 2 (PMCA2), a high-affinity P-type ATPase that extrudes cytosolic Ca2+ to maintain calcium homeostasis after signaling events. By shaping the amplitude and duration of Ca2+-dependent pathways, PMCA2 influences processes such as synaptic transmission, sensory signaling, and activity-dependent gene regulation, and contributes to the coupling between calcium influx and downstream effectors. PMCA2 activity is integrated with calmodulin regulation and broader ion-transport and membrane potential networks that coordinate intracellular Ca2+ dynamics. Genetic and expression perturbations in ATP2B2 have been associated with disorders affecting auditory and neural function, supporting its relevance as a target for mechanistic studies of calcium-dependent physiology.
PMCA2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ATP2B2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ATP2B2. 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 ATP2B2 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 ATP2B2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.