Nox4 Double Nickase Plasmid (m): sc-424443-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Nox4 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
- Nox4 Double Nickase Plasmid (m) and Nox4 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Nox4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Nox4 Double Nickase Plasmid (m) | sc-424443-NIC | 20 µg | $410.00 | |||
Nox4 Double Nickase Plasmid (m2) | sc-424443-NIC-2 | 20 µg | $410.00 |
Nox4 (NADPH oxidase 4) is a catalytic ROS-generating enzyme in mouse cells that constitutively produces hydrogen peroxide to shape redox signaling. Nox4-derived oxidants modulate pathways including TGF-β/SMAD, MAPK, PI3K–AKT, and NF-κB, influencing transcriptional programs that govern differentiation, extracellular matrix remodeling, and stress responses. In vascular, renal, pulmonary, and cardiac contexts, dysregulated Nox4 activity has been linked to oxidative stress–dependent remodeling, inflammation, and fibrotic processes. As a redox regulator, Nox4 is frequently studied for its effects on endothelial function, fibroblast activation, and metabolic adaptation under hypoxia or inflammatory stimuli.
Nox4 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Nox4 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Nox4. 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 Nox4 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 Nox4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.