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.
SIRT5 Double Nickase Plasmid (h): sc-416994-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SIRT5 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
- SIRT5 Double Nickase Plasmid (h) and SIRT5 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SIRT5. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: SIRT5 Antibody (G-2): sc-271635
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SIRT5 Double Nickase Plasmid (h) | sc-416994-NIC | 20 µg | $410.00 | |||
SIRT5 Double Nickase Plasmid (h2) | sc-416994-NIC-2 | 20 µg | $410.00 |
SIRT5 encodes a mitochondrial NAD+-dependent sirtuin deacylase that preferentially removes succinyl, malonyl, and glutaryl lysine modifications, thereby tuning enzyme activity across central metabolism. By regulating pathways such as the urea cycle, fatty acid oxidation, and oxidative phosphorylation, SIRT5 helps maintain mitochondrial homeostasis and redox balance under nutrient and stress fluctuations. Altered SIRT5 activity has been linked to metabolic remodeling, oxidative stress responses, and mitochondrial dysfunction observed across cancer and cardiometabolic research contexts. As a post-translational regulator of mitochondrial proteins, SIRT5 is frequently studied for its impact on proteome acylation states and downstream signaling networks that couple energy status to cellular adaptation.
SIRT5 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SIRT5 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SIRT5. 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 SIRT5 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 SIRT5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.