ACOX1 Double Nickase Plasmid (h): sc-401690-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACOX1 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
- ACOX1 Double Nickase Plasmid (h) and ACOX1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ACOX1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ACOX1 Antibody (153CT43.1.1): sc-517306
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACOX1 Double Nickase Plasmid (h) | sc-401690-NIC | 20 µg | $410.00 | |||
ACOX1 Double Nickase Plasmid (h2) | sc-401690-NIC-2 | 20 µg | $410.00 |
ACOX1 encodes acyl-CoA oxidase 1, the rate-limiting peroxisomal enzyme that catalyzes the first step of very-long-chain fatty acid β-oxidation and generates hydrogen peroxide as a byproduct. Through its role in peroxisomal lipid catabolism, ACOX1 helps maintain cellular lipid homeostasis and interfaces with redox regulation and metabolic signaling pathways. Altered ACOX1 activity has been linked to peroxisomal dysfunction phenotypes, including accumulation of very-long-chain fatty acids and secondary effects on mitochondrial metabolism. Dysregulation of peroxisomal β-oxidation and oxidative stress pathways involving ACOX1 is relevant to studies of neurodevelopment, liver metabolism, and inflammatory responses.
ACOX1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ACOX1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ACOX1. 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 ACOX1 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 ACOX1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.