PLRP2 Double Nickase Plasmid (h): sc-409664-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PLRP2 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
- PLRP2 Double Nickase Plasmid (h) and PLRP2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PNLIPRP2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: PLRP2 Antibody (D-1): sc-376236
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PLRP2 Double Nickase Plasmid (h) | sc-409664-NIC | 20 µg | $410.00 |
PNLIPRP2 encodes pancreatic lipase-related protein 2 (PLRP2), a secreted lipase that contributes to the hydrolysis of dietary triacylglycerols and related lipids in the intestinal lumen. PLRP2 participates in digestive and metabolic processes that influence intestinal lipid absorption, downstream chylomicron production, and systemic energy homeostasis. Variation in digestive lipase activity is relevant to studies of malabsorption phenotypes and metabolic dysregulation, and PLRP2 is often examined alongside other pancreatic enzymes to understand coordinated exocrine pancreas function. In biomedical research, PNLIPRP2 provides a tractable node for investigating lipid handling at the gut–pancreas interface and the consequences of altered luminal lipolysis on inflammatory and metabolic pathways.
PLRP2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PNLIPRP2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PNLIPRP2. 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 PNLIPRP2 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 PNLIPRP2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.