apoF Double Nickase Plasmid (h): sc-407655-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- apoF 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
- apoF Double Nickase Plasmid (h) and apoF Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting APOF. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
apoF Double Nickase Plasmid (h) | sc-407655-NIC | 20 µg | $410.00 | |||
apoF Double Nickase Plasmid (h2) | sc-407655-NIC-2 | 20 µg | $410.00 |
APOF encodes apolipoprotein F (apoF), a secreted glycoprotein associated with HDL and LDL particles that modulates lipoprotein remodeling and cholesterol transport. apoF influences lipid exchange processes in plasma, including pathways connected to lecithin–cholesterol acyltransferase activity and lipoprotein receptor–mediated clearance, thereby shaping systemic lipid homeostasis. Variation in APOF expression and function has been linked to altered circulating lipid profiles and cardiometabolic risk traits, making it relevant for studying dyslipidemia-associated mechanisms. In cell and animal models, APOF provides a tractable node to interrogate HDL biology, hepatic lipid handling, and gene–environment interactions affecting lipid metabolism.
apoF Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the APOF locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within APOF. 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 APOF 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 APOF-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.