ABCD2 Double Nickase Plasmid (h): sc-405099-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ABCD2 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
- ABCD2 Double Nickase Plasmid (h) and ABCD2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ABCD2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ABCD2 Double Nickase Plasmid (h) | sc-405099-NIC | 20 µg | $410.00 | |||
ABCD2 Double Nickase Plasmid (h2) | sc-405099-NIC-2 | 20 µg | $410.00 |
ABCD2 encodes an ATP-binding cassette transporter localized to the peroxisomal membrane that imports very-long-chain fatty acyl-CoAs for peroxisomal β-oxidation. By supporting lipid catabolism and peroxisome–mitochondria metabolic crosstalk, ABCD2 contributes to cellular lipid homeostasis, redox balance, and membrane lipid remodeling. Its activity overlaps with other peroxisomal ABC transporters, making it a key node in pathways governing very-long-chain fatty acid handling. Dysregulation of peroxisomal fatty acid transport and β-oxidation is implicated in neuroinflammatory and neurodegenerative contexts and is used as a mechanistic framework for studying peroxisome-related lipid stress.
ABCD2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ABCD2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ABCD2. 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 ABCD2 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 ABCD2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.