ABCA3 Double Nickase Plasmid (h): sc-402388-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ABCA3 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
- ABCA3 Double Nickase Plasmid (h) and ABCA3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ABCA3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ABCA3 Double Nickase Plasmid (h) | sc-402388-NIC | 20 µg | $410.00 | |||
ABCA3 Double Nickase Plasmid (h2) | sc-402388-NIC-2 | 20 µg | $410.00 |
ABCA3 encodes an ATP-binding cassette transporter that localizes to lamellar bodies in alveolar type II epithelial cells, where it uses ATP hydrolysis to drive phospholipid translocation required for pulmonary surfactant maturation and storage. By regulating lamellar body biogenesis, vesicle trafficking, and lipid homeostasis, ABCA3 supports alveolar stability and efficient gas exchange. Disruption of ABCA3 function is linked to impaired surfactant metabolism and is widely studied in the context of inherited and acquired interstitial lung disease phenotypes. As a membrane transporter with cell type–restricted expression, ABCA3 is also used as a model for investigating proteostasis, ER quality control, and lipid transport pathways in epithelial biology.
ABCA3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ABCA3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ABCA3. 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 ABCA3 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 ABCA3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.