Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Apolipoprotein A I/APOA1 Double Nickase Plasmid (h): sc-400499-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Apolipoprotein A I/APOA1 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
- Apolipoprotein A I/APOA1 Double Nickase Plasmid (h) and Apolipoprotein A I/APOA1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting APOA1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Apolipoprotein A I/APOA1 Antibody (B-10): sc-376818
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Apolipoprotein A I/APOA1 Double Nickase Plasmid (h) | sc-400499-NIC | 20 µg | $410.00 | |||
Apolipoprotein A I/APOA1 Double Nickase Plasmid (h2) | sc-400499-NIC-2 | 20 µg | $410.00 |
Human APOA1 encodes apolipoprotein A-I, the major protein component of high-density lipoprotein (HDL) particles and a central mediator of reverse cholesterol transport. APOA1 interacts with ABCA1 and ABCG1 to promote cellular cholesterol and phospholipid efflux, driving nascent HDL biogenesis and supporting lecithin–cholesterol acyltransferase (LCAT)-dependent HDL maturation. Through these processes, APOA1 influences lipid homeostasis, macrophage foam cell formation, and inflammatory signaling in vascular and hepatic contexts. Altered APOA1 expression or function is associated with dyslipidemia and atherosclerosis-related phenotypes, making it a key target for mechanistic studies of lipoprotein metabolism.
Apolipoprotein A I/APOA1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the APOA1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within APOA1. 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 APOA1 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 APOA1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.