NSUN4 Double Nickase Plasmid (m): sc-428269-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NSUN4 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
- NSUN4 Double Nickase Plasmid (m) and NSUN4 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Nsun4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NSUN4 Double Nickase Plasmid (m) | sc-428269-NIC | 20 µg | $410.00 |
Nsun4 encodes NSUN4, a mitochondrial RNA cytosine-5 methyltransferase that methylates mt-rRNA and supports mitochondrial ribosome biogenesis and translation. Through coordination with mitochondrial transcription/translation machinery, NSUN4 helps maintain oxidative phosphorylation capacity and respiratory chain function, linking it to cellular energy metabolism and mitochondrial quality control. Perturbation of NSUN4 activity is expected to alter mitochondrial protein synthesis and bioenergetic signaling pathways that influence stress responses and cell fate decisions. As a result, Nsun4 is frequently studied in contexts where mitochondrial dysfunction contributes to disease-relevant phenotypes, including neurodegeneration, cardiometabolic imbalance, and developmental defects.
NSUN4 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Nsun4 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Nsun4. 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 Nsun4 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 Nsun4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.