ATP5I Double Nickase Plasmid (h): sc-410696-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATP5I 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
- ATP5I Double Nickase Plasmid (h) and ATP5I Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ATP5I. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ATP5I Double Nickase Plasmid (h) | sc-410696-NIC | 20 µg | $410.00 | |||
ATP5I Double Nickase Plasmid (h2) | sc-410696-NIC-2 | 20 µg | $410.00 |
ATP5I encodes a small, integral membrane subunit of mitochondrial ATP synthase (complex V) that contributes to proper assembly and stability of the F0 sector and supports oxidative phosphorylation. By enabling efficient coupling of the proton motive force to ATP production, ATP5I helps maintain cellular energy homeostasis, mitochondrial membrane potential, and redox balance. Perturbation of ATP synthase subunits can impact electron transport chain function, increase reactive oxygen species, and alter metabolic signaling pathways that influence apoptosis and stress responses. Dysregulated mitochondrial bioenergetics involving complex V components has been implicated in a range of mitochondrial disorders and broader phenotypes associated with energy-demanding tissues.
ATP5I Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ATP5I locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ATP5I. 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 ATP5I 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 ATP5I-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.