SIRT4 Double Nickase Plasmid (h): sc-401187-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SIRT4 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
- SIRT4 Double Nickase Plasmid (h) and SIRT4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SIRT4. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: SIRT4 Antibody (95.1): sc-135797
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SIRT4 Double Nickase Plasmid (h) | sc-401187-NIC | 20 µg | $410.00 | |||
SIRT4 Double Nickase Plasmid (h2) | sc-401187-NIC-2 | 20 µg | $410.00 |
SIRT4 encodes a mitochondrial sirtuin that uses NAD+ to regulate post-translational modifications, linking cellular redox state to metabolic control. SIRT4 modulates mitochondrial fuel selection through inhibition of glutamate dehydrogenase and regulation of amino acid anaplerosis, with downstream effects on the TCA cycle, oxidative phosphorylation, and reactive oxygen species homeostasis. It also influences lipid metabolism, insulin secretion pathways, and cellular stress responses through coordinated mitochondrial signaling. Dysregulated SIRT4 activity has been associated with altered metabolic phenotypes and has been investigated in contexts including cancer metabolism, neurodegeneration, and cardiometabolic disease models.
SIRT4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SIRT4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SIRT4. 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 SIRT4 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 SIRT4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.