PC-PLD3 Double Nickase Plasmid (h): sc-406631-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PC-PLD3 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
- PC-PLD3 Double Nickase Plasmid (h) and PC-PLD3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PLD3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PC-PLD3 Double Nickase Plasmid (h) | sc-406631-NIC | 20 µg | $410.00 | |||
PC-PLD3 Double Nickase Plasmid (h2) | sc-406631-NIC-2 | 20 µg | $410.00 |
PLD3 (phospholipase D family member 3) encodes a type II transmembrane protein enriched in endolysosomal compartments and implicated in membrane lipid metabolism and vesicular trafficking. PC-PLD3 has been linked to regulation of endosome–lysosome function, proteostasis, and processing of membrane-associated substrates, processes that intersect with neuronal homeostasis and innate immune signaling. Genetic and expression studies have associated PLD3 with neurodegenerative disease risk and altered amyloidogenic pathways, making it a target of interest in models of neuronal stress, lysosomal dysfunction, and age-related pathology. In cellular systems, perturbation of PLD3 can be used to probe how lipid- and vesicle-dependent mechanisms shape protein turnover and signaling outputs.
PC-PLD3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PLD3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PLD3. 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 PLD3 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 PLD3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.