ABCA2 Double Nickase Plasmid (h): sc-405934-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ABCA2 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
- ABCA2 Double Nickase Plasmid (h) and ABCA2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ABCA2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ABCA2 Double Nickase Plasmid (h) | sc-405934-NIC | 20 µg | $410.00 | |||
ABCA2 Double Nickase Plasmid (h2) | sc-405934-NIC-2 | 20 µg | $410.00 |
ABCA2 encodes an ATP-binding cassette (ABC) transporter predominantly localized to endolysosomal membranes, where it contributes to intracellular lipid handling and membrane homeostasis. By coupling ATP hydrolysis to substrate transport, ABCA2 influences cholesterol and sphingolipid trafficking, vesicular dynamics, and broader proteostasis pathways that intersect with endocytic and lysosomal function. Altered ABCA2 expression has been linked to neurobiology-relevant processes and lipid dysregulation, and it is frequently studied in contexts where membrane composition impacts signaling and cellular stress responses. As a large multi-pass transporter, ABCA2 also serves as a model for investigating ABC transporter regulation, subcellular localization, and the consequences of lipid transport perturbation.
ABCA2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ABCA2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ABCA2. 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 ABCA2 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 ABCA2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.