CTRL Double Nickase Plasmid (h): sc-410749-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CTRL 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
- CTRL Double Nickase Plasmid (h) and CTRL Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CTRL. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CTRL Double Nickase Plasmid (h) | sc-410749-NIC | 20 µg | $410.00 | |||
CTRL Double Nickase Plasmid (h2) | sc-410749-NIC-2 | 20 µg | $410.00 |
Human CTRL encodes chymotrypsin-like protease CTRL, a serine endopeptidase that contributes to proteolytic processing of proteins and peptides in digestive and extracellular environments. As a trypsin-family protease, CTRL activity integrates with protease activation cascades and regulated proteolysis that can influence peptide hormone maturation, nutrient handling, and local signaling. Dysregulated serine protease activity is broadly linked to inflammatory responses and tissue remodeling, making CTRL a useful model for studying protease network balance and protease–substrate specificity. Experimental modulation of CTRL supports mechanistic work on protease-mediated pathway regulation and downstream effects on cellular stress and inflammatory signaling.
CTRL Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CTRL locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CTRL. 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 CTRL 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 CTRL-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.