NEIL3 Double Nickase Plasmid (h): sc-406572-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NEIL3 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
- NEIL3 Double Nickase Plasmid (h) and NEIL3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting NEIL3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NEIL3 Double Nickase Plasmid (h) | sc-406572-NIC | 20 µg | $410.00 | |||
NEIL3 Double Nickase Plasmid (h2) | sc-406572-NIC-2 | 20 µg | $410.00 |
NEIL3 (endonuclease VIII-like 3) is a DNA glycosylase/AP lyase that initiates base excision repair by recognizing and removing oxidized DNA lesions, with a preference for lesions in single-stranded or replication-associated DNA structures. It contributes to genome maintenance during S phase by limiting replication stress and promoting fork stability, linking NEIL3 activity to DNA damage response coordination and cell-cycle progression. NEIL3 function intersects with pathways regulating oxidative stress, chromatin-associated repair, and maintenance of genomic integrity in proliferative cells. Altered NEIL3 expression or function has been associated with dysregulated DNA repair capacity and genomic instability phenotypes relevant to studies of tumor biology and neurodegeneration-associated oxidative damage.
NEIL3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the NEIL3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within NEIL3. 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 NEIL3 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 NEIL3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.