C6orf105 Double Nickase Plasmid (h): sc-413707-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- C6orf105 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
- C6orf105 Double Nickase Plasmid (h) and C6orf105 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ADTRP. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
C6orf105 Double Nickase Plasmid (h) | sc-413707-NIC | 20 µg | $410.00 | |||
C6orf105 Double Nickase Plasmid (h2) | sc-413707-NIC-2 | 20 µg | $410.00 |
ADTRP (also known as C6orf105) encodes androgen-dependent TFPI-regulating protein, a membrane-associated factor implicated in vascular homeostasis and regulation of tissue factor pathway inhibitor (TFPI) activity. It has been linked to endothelial function and coagulation-related processes, with reported connections to extracellular protease regulation and cell surface signaling. Genetic and expression studies associate ADTRP variation or dysregulation with thrombotic and cardiovascular phenotypes, making it a relevant target for mechanistic investigation in vascular biology. In human cell models, perturbation of C6orf105 supports interrogation of pathways influencing hemostasis, endothelial responses, and inflammation-associated remodeling.
C6orf105 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ADTRP locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ADTRP. 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 ADTRP 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 ADTRP-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.