SIRT4 Double Nickase Plasmid (r): sc-437316-NIC
- Target species: rat
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SIRT4 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
- SIRT4 Double Nickase Plasmid (r) and SIRT4 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 | |
SIRT4 Double Nickase Plasmid (r) | sc-437316-NIC | 20 µg | $410.00 | |||
SIRT4 Double Nickase Plasmid (r2) | sc-437316-NIC-2 | 20 µg | $410.00 |
SIRT4 is a mitochondrial sirtuin that functions as an NAD+-dependent regulator of metabolic homeostasis, influencing nutrient sensing, mitochondrial enzyme activity, and cellular energy flux. In rat cells, SIRT4 modulates processes such as glutamine utilization, fatty acid oxidation, and oxidative stress responses through post-translational control of key mitochondrial targets, linking it to broader AMPK–mTOR signaling and mitochondrial quality control pathways. Altered SIRT4 activity has been studied in contexts of mitochondrial dysfunction and metabolic remodeling, where changes in redox balance and bioenergetic capacity can influence susceptibility to stress. These features make SIRT4 a useful node for mechanistic studies of mitochondrial regulation, metabolic reprogramming, and stress-adaptive signaling networks.
SIRT4 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.