SIRT2 Double Nickase Plasmid (h): sc-400590-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SIRT2 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
- SIRT2 Double Nickase Plasmid (h) and SIRT2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SIRT2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: SIRT2 Antibody (A-5): sc-28298
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SIRT2 Double Nickase Plasmid (h) | sc-400590-NIC | 20 µg | $410.00 | |||
SIRT2 Double Nickase Plasmid (h2) | sc-400590-NIC-2 | 20 µg | $410.00 |
SIRT2 encodes a NAD⁺-dependent deacetylase that primarily localizes to the cytoplasm and modulates protein acetylation states governing microtubule dynamics, cell-cycle progression, and cellular stress responses. By deacetylating substrates such as α-tubulin and metabolic regulators, SIRT2 helps coordinate cytoskeletal remodeling, mitotic fidelity, and metabolic adaptation, linking its activity to pathways influenced by NAD⁺ availability and redox balance. Altered SIRT2 function has been investigated in the context of neurodegeneration, inflammation, and cancer-related phenotypes where changes in acetylation-dependent signaling can impact differentiation, survival, and genomic stability. As a member of the sirtuin family, SIRT2 is frequently studied for its role in integrating nutrient sensing with epigenetic and post-translational control of cellular programs.
SIRT2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SIRT2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SIRT2. 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 SIRT2 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 SIRT2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.