ACO2 Double Nickase Plasmid (h): sc-404434-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACO2 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
- ACO2 Double Nickase Plasmid (h) and ACO2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ACO2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ACO2 Antibody (775F2I): sc-517651
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACO2 Double Nickase Plasmid (h) | sc-404434-NIC | 20 µg | $410.00 | |||
ACO2 Double Nickase Plasmid (h2) | sc-404434-NIC-2 | 20 µg | $410.00 |
ACO2 encodes mitochondrial aconitase 2, a [4Fe–4S] iron–sulfur enzyme that catalyzes the reversible isomerization of citrate to isocitrate in the tricarboxylic acid (TCA) cycle. By supporting oxidative metabolism, NADH production, and mitochondrial ATP generation, ACO2 contributes to redox homeostasis and cellular bioenergetic capacity. ACO2 activity is linked to mitochondrial stress responses and sensitivity to reactive oxygen species through iron–sulfur cluster integrity. Altered ACO2 function has been associated with metabolic dysfunction and mitochondrial disease phenotypes, making it a useful target for studying bioenergetic rewiring in cancer and neurodegeneration models.
ACO2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ACO2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ACO2. 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 ACO2 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 ACO2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.