OCT1 Double Nickase Plasmid (h): sc-402232-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- OCT1 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
- OCT1 Double Nickase Plasmid (h) and OCT1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLC22A1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
OCT1 Double Nickase Plasmid (h) | sc-402232-NIC | 20 µg | $410.00 | |||
OCT1 Double Nickase Plasmid (h2) | sc-402232-NIC-2 | 20 µg | $410.00 |
SLC22A1 encodes the human organic cation transporter 1 (OCT1), a polyspecific uptake transporter predominantly localized to the plasma membrane where it mediates sodium-independent import of endogenous amines and diverse xenobiotic cations. OCT1 activity influences cellular disposition of organic cations and contributes to hepatic and epithelial transport processes that shape intracellular exposure, metabolic coupling, and detoxification. Variation in SLC22A1 expression or sequence has been associated with altered transporter function and inter-individual differences in drug handling, making it relevant to pharmacogenomics, toxicology, and transporter biology. In research settings, OCT1 is commonly studied in the context of membrane transport regulation, substrate specificity, and pathways governing cellular uptake and clearance.
OCT1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLC22A1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SLC22A1. 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 SLC22A1 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 SLC22A1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.