PLA1A Double Nickase Plasmid (h): sc-412191-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PLA1A 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
- PLA1A Double Nickase Plasmid (h) and PLA1A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PLA1A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PLA1A Double Nickase Plasmid (h) | sc-412191-NIC | 20 µg | $410.00 |
PLA1A (phospholipase A1 member A) encodes a secreted lysophospholipase that hydrolyzes phosphatidylserine to generate lysophosphatidylserine and free fatty acids, shaping the composition of bioactive lipid mediators in the extracellular milieu. Through modulation of lysophospholipid signaling, PLA1A can influence membrane remodeling, lipid metabolic flux, and receptor-dependent pathways that regulate inflammatory and immune cell behavior. Altered PLA1A activity and downstream lysophospholipid profiles have been linked to dysregulated inflammation and cardiometabolic phenotypes, supporting its relevance to studies of atherosclerosis, metabolic syndrome, and related vascular biology. As a circulating enzyme, PLA1A is also useful for interrogating endocrine-like lipid signaling and systemic biomarkers in human cell and tissue models.
PLA1A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PLA1A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PLA1A. 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 PLA1A 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 PLA1A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.