TOX3 Double Nickase Plasmid (h): sc-411992-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TOX3 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
- TOX3 Double Nickase Plasmid (h) and TOX3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TOX3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TOX3 Double Nickase Plasmid (h) | sc-411992-NIC | 20 µg | $410.00 | |||
TOX3 Double Nickase Plasmid (h2) | sc-411992-NIC-2 | 20 µg | $410.00 |
TOX3 encodes a high mobility group (HMG) box transcription factor that binds DNA and modulates chromatin structure to regulate gene expression programs linked to cellular differentiation and stimulus-responsive transcription. It is implicated in neuronal development and activity-dependent gene regulation, and participates in broader transcriptional networks that influence cell fate decisions and stress responses. Genetic and expression studies associate TOX3 with disease-relevant pathways, including susceptibility loci in hormone-responsive cancers and alterations observed in neuropsychiatric and neurodegenerative contexts. These features make TOX3 a useful target for dissecting transcriptional control mechanisms and downstream gene networks in human cell models.
TOX3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TOX3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TOX3. 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 TOX3 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 TOX3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.