ANT2 Double Nickase Plasmid (m): sc-419113-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ANT2 Double Nickase Plasmid (m) 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
- ANT2 Double Nickase Plasmid (m) and ANT2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Slc25a5. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ANT2 Double Nickase Plasmid (m) | sc-419113-NIC | 20 µg | $410.00 | |||
ANT2 Double Nickase Plasmid (m2) | sc-419113-NIC-2 | 20 µg | $410.00 |
Slc25a5 encodes the mitochondrial ADP/ATP translocase ANT2, a key inner membrane carrier that exchanges cytosolic ADP for matrix ATP to sustain oxidative phosphorylation and cellular energy balance. ANT2 activity couples the adenine nucleotide pool to mitochondrial membrane potential, linking metabolic flux with processes such as mitochondrial biogenesis, apoptosis susceptibility, and reactive oxygen species homeostasis. In mouse systems, ANT2 is frequently studied in contexts of metabolic remodeling, proliferative energy demand, and mitochondrial stress responses. Dysregulation of adenine nucleotide transport and mitochondrial bioenergetics is relevant to neuromuscular and cardiometabolic phenotypes and to broader mitochondrial dysfunction models.
ANT2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Slc25a5 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Slc25a5. 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 Slc25a5 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 Slc25a5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.