ATP5G2 Double Nickase Plasmid (h): sc-403484-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATP5G2 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
- ATP5G2 Double Nickase Plasmid (h) and ATP5G2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ATP5G2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ATP5G2 Double Nickase Plasmid (h) | sc-403484-NIC | 20 µg | $410.00 | |||
ATP5G2 Double Nickase Plasmid (h2) | sc-403484-NIC-2 | 20 µg | $410.00 |
ATP5G2 encodes a membrane-embedded subunit of mitochondrial ATP synthase (Complex V) that contributes to the Fo sector and supports proton translocation required for oxidative phosphorylation and ATP production. By linking the mitochondrial proton motive force to ATP synthesis, ATP5G2 influences cellular energy homeostasis, respiratory efficiency, and metabolic adaptation during changing nutrient and oxygen conditions. Altered mitochondrial ATP synthase function can contribute to bioenergetic stress, reactive oxygen species imbalance, and impaired mitochondrial dynamics, processes implicated in a range of disorders with mitochondrial dysfunction. ATP5G2 is therefore relevant for studies of electron transport chain coupling, mitochondrial membrane potential regulation, and energy-dependent signaling pathways.
ATP5G2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ATP5G2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ATP5G2. 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 ATP5G2 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 ATP5G2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.