NOS2/iNOS Double Nickase Plasmid (h): sc-400066-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NOS2/iNOS 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
- NOS2/iNOS Double Nickase Plasmid (h) and NOS2/iNOS Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting NOS2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: NOS2/iNOS Antibody (C-11): sc-7271
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NOS2/iNOS Double Nickase Plasmid (h) | sc-400066-NIC | 20 µg | $410.00 | |||
NOS2/iNOS Double Nickase Plasmid (h2) | sc-400066-NIC-2 | 20 µg | $410.00 |
Human NOS2 encodes inducible nitric oxide synthase (iNOS), a Ca2+-independent enzyme that generates high-output nitric oxide from L-arginine during inflammatory stimulation. iNOS-derived NO modulates innate immune signaling, antimicrobial defense, and oxidative/nitrosative stress through effects on redox homeostasis, S-nitrosylation, and reactive nitrogen species formation. NOS2 expression is regulated by cytokine- and pattern-recognition receptor–driven pathways including NF-κB, JAK/STAT, and MAPK cascades. Dysregulated NOS2 activity has been linked to chronic inflammation and tissue injury and is frequently studied in the context of tumor microenvironment biology, neuroinflammation, and cardiometabolic stress responses.
NOS2/iNOS Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the NOS2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within NOS2. 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 NOS2 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 NOS2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.