apoA Double Nickase Plasmid (h): sc-404800-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- apoA 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
- apoA Double Nickase Plasmid (h) and apoA Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LPA. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
apoA Double Nickase Plasmid (h) | sc-404800-NIC | 20 µg | $410.00 | |||
apoA Double Nickase Plasmid (h2) | sc-404800-NIC-2 | 20 µg | $410.00 |
Human LPA encodes apolipoprotein(a) (apoA), a liver-derived glycoprotein that covalently associates with apolipoprotein B-100 to form lipoprotein(a), a particle that links lipid transport with coagulation-related processes through its plasminogen-like kringle domains. Variants in LPA influence circulating Lp(a) levels and modulate pathways involved in extracellular proteolysis, vascular matrix remodeling, and inflammatory signaling. Altered apoA/Lp(a) biology is used as a molecular context for studying atherothrombosis mechanisms and lipid-associated vascular phenotypes. As a result, LPA is a common target in functional genomics studies examining lipid metabolism, endothelial responses, and hepatocyte secretory pathways.
apoA Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LPA locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LPA. 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 LPA 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 LPA-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.