SIRT6 Double Nickase Plasmid (m): sc-424467-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SIRT6 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
- SIRT6 Double Nickase Plasmid (m) and SIRT6 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Sirt6. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: SIRT6 Antibody (6C9-D10-D3): sc-517556
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SIRT6 Double Nickase Plasmid (m) | sc-424467-NIC | 20 µg | $410.00 | |||
SIRT6 Double Nickase Plasmid (m2) | sc-424467-NIC-2 | 20 µg | $410.00 |
Sirt6 encodes the NAD⁺-dependent deacylase and mono-ADP-ribosyltransferase SIRT6, a chromatin-associated enzyme that regulates transcription, genome stability, and metabolic homeostasis. In mouse cells, SIRT6 modulates histone H3 lysine 9 and 56 deacetylation, linking chromatin state to DNA damage responses, telomere maintenance, and replication-associated repair. It intersects with pathways controlling oxidative stress, inflammation, and glucose and lipid metabolism, including NF-κB- and HIF1A-associated transcriptional programs. Dysregulated SIRT6 activity is widely used as a mechanistic entry point for studying aging-related phenotypes, metabolic dysfunction, and oncogenic transcriptional rewiring in relevant murine models.
SIRT6 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Sirt6 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Sirt6. 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 Sirt6 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 Sirt6-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.