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 (r): sc-437315-NIC
- Target species: rat
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SIRT3 Double Nickase Plasmid (r) 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 (r) and SIRT3 Double Nickase Plasmid (r2) encode distinct paired gRNA designs targeting . One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SIRT3 Double Nickase Plasmid (r) | sc-437315-NIC | 20 µg | $410.00 | |||
SIRT3 Double Nickase Plasmid (r2) | sc-437315-NIC-2 | 20 µg | $410.00 |
SIRT3 encodes a mitochondrial NAD+-dependent deacetylase that regulates oxidative metabolism and mitochondrial protein homeostasis by deacetylating enzymes involved in fatty acid oxidation, the TCA cycle, and the electron transport chain. Through control of mitochondrial redox balance, SIRT3 modulates reactive oxygen species detoxification and supports adaptive responses to energetic and oxidative stress. Altered SIRT3 activity has been linked to mitochondrial dysfunction and dysregulated bioenergetics in contexts such as metabolic disease, cardiac stress remodeling, neurodegeneration, and tumor metabolism, making it a common target for mechanistic studies in rat models. These pathways connect SIRT3 to mitochondrial quality control, stress signaling, and apoptosis-related processes that are frequently interrogated in biomedical research.
SIRT3 Double Nickase Plasmid (r) consists of a matched pair of plasmids engineered for high-specificity editing of the locus in rat cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within . 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 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 -disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.