ABCD1 Double Nickase Plasmid (h): sc-405301-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ABCD1 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
- ABCD1 Double Nickase Plasmid (h) and ABCD1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ABCD1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ABCD1 Double Nickase Plasmid (h) | sc-405301-NIC | 20 µg | $410.00 | |||
ABCD1 Double Nickase Plasmid (h2) | sc-405301-NIC-2 | 20 µg | $410.00 |
ABCD1 encodes a peroxisomal ATP-binding cassette transporter that imports very-long-chain fatty acyl-CoAs into peroxisomes for β-oxidation, helping maintain lipid homeostasis and membrane composition. Through its role in peroxisomal fatty acid catabolism, ABCD1 intersects with pathways controlling redox balance, mitochondrial–peroxisome metabolic coupling, and inflammatory signaling linked to lipid accumulation. Loss-of-function variants in human ABCD1 are associated with X-linked adrenoleukodystrophy, where impaired peroxisomal VLCFA degradation leads to elevated VLCFAs and downstream cellular stress phenotypes. ABCD1 perturbation is therefore widely used to model peroxisomal dysfunction and lipid-driven cellular pathology in relevant cell types.
ABCD1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ABCD1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ABCD1. 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 ABCD1 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 ABCD1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.