INDOL1 Double Nickase Plasmid (h): sc-403856-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- INDOL1 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
- INDOL1 Double Nickase Plasmid (h) and INDOL1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IDO2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
INDOL1 Double Nickase Plasmid (h) | sc-403856-NIC | 20 µg | $410.00 | |||
INDOL1 Double Nickase Plasmid (h2) | sc-403856-NIC-2 | 20 µg | $410.00 |
Human IDO2 (INDOL1) encodes an indoleamine 2,3-dioxygenase family enzyme that catalyzes oxidative metabolism of tryptophan along the kynurenine pathway, influencing local amino acid availability and downstream bioactive metabolites. Through regulation of tryptophan catabolism, IDO2 can affect immune signaling, redox balance, and cellular stress responses, with context-dependent impacts on antigen-presenting cell function and inflammatory pathways. Altered kynurenine pathway activity and IDO2 expression have been reported in settings of chronic inflammation and immune dysregulation, and are studied for their associations with tumor-immune interactions and neuroinflammatory processes. IDO2 is therefore a useful node for dissecting metabolic control of immune phenotypes and pathway crosstalk in human cell models.
INDOL1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IDO2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IDO2. 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 IDO2 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 IDO2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.