CTR1 Double Nickase Plasmid (h): sc-417947-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CTR1 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
- CTR1 Double Nickase Plasmid (h) and CTR1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLC31A1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CTR1 Double Nickase Plasmid (h) | sc-417947-NIC | 20 µg | $410.00 | |||
CTR1 Double Nickase Plasmid (h2) | sc-417947-NIC-2 | 20 µg | $410.00 |
SLC31A1 encodes the high-affinity copper transporter CTR1, a plasma membrane protein that mediates cellular uptake of copper ions required for essential cuproenzyme activity. By controlling intracellular copper availability, CTR1 influences redox homeostasis, mitochondrial respiration, and oxidative stress responses, and it contributes to the regulation of metal-dependent signaling and metabolic pathways. Perturbation of SLC31A1/CTR1 function can disrupt copper balance, alter antioxidant capacity, and impact pathways linked to proteostasis and cellular viability. Dysregulated copper transport and CTR1 expression have been associated with altered metal homeostasis phenotypes relevant to neurodegeneration, liver biology, and tumor cell metabolism in research settings.
CTR1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLC31A1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SLC31A1. 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 SLC31A1 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 SLC31A1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.