NDUFS4 Double Nickase Plasmid (h): sc-405184-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NDUFS4 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
- NDUFS4 Double Nickase Plasmid (h) and NDUFS4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting NDUFS4. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: NDUFS4 Antibody (A-7): sc-514002
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NDUFS4 Double Nickase Plasmid (h) | sc-405184-NIC | 20 µg | $410.00 |
NDUFS4 encodes an accessory subunit of mitochondrial respiratory chain complex I (NADH:ubiquinone oxidoreductase) that supports complex I assembly and stability within the inner mitochondrial membrane. By enabling efficient electron transfer from NADH to ubiquinone, NDUFS4 contributes to oxidative phosphorylation, maintenance of mitochondrial membrane potential, and regulation of cellular redox balance. Disruption of NDUFS4 function is linked to impaired complex I activity, altered reactive oxygen species handling, and metabolic remodeling that can affect bioenergetic signaling networks. Variants in NDUFS4 are associated with mitochondrial complex I deficiency phenotypes, making it a relevant target for mechanistic studies of mitochondrial dysfunction and stress responses.
NDUFS4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the NDUFS4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within NDUFS4. 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 NDUFS4 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 NDUFS4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.