Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
SIRT3 Double Nickase Plasmid (m): sc-425704-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SIRT3 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
- SIRT3 Double Nickase Plasmid (m) and SIRT3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Sirt3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: SIRT3 Antibody (F-10): sc-365175
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SIRT3 Double Nickase Plasmid (m) | sc-425704-NIC | 20 µg | $410.00 | |||
SIRT3 Double Nickase Plasmid (m2) | sc-425704-NIC-2 | 20 µg | $410.00 |
Mouse Sirt3 encodes the mitochondrial NAD⁺-dependent deacetylase SIRT3, a central regulator of mitochondrial protein acetylation and oxidative metabolism. SIRT3 modulates pathways including fatty acid β-oxidation, the TCA cycle, electron transport chain activity, and reactive oxygen species detoxification through deacetylation of key mitochondrial enzymes. By shaping mitochondrial respiration, redox balance, and cellular stress responses, SIRT3 influences metabolic adaptation in tissues with high energy demand. Altered SIRT3 activity has been associated with mitochondrial dysfunction phenotypes relevant to metabolic stress, neurodegeneration models, and inflammation-linked damage in preclinical research.
SIRT3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Sirt3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Sirt3. 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 Sirt3 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 Sirt3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.