quiescin Q6 Double Nickase Plasmid (h): sc-405059-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- quiescin Q6 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
- quiescin Q6 Double Nickase Plasmid (h) and quiescin Q6 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting QSOX1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
quiescin Q6 Double Nickase Plasmid (h) | sc-405059-NIC | 20 µg | $410.00 | |||
quiescin Q6 Double Nickase Plasmid (h2) | sc-405059-NIC-2 | 20 µg | $410.00 |
QSOX1 encodes quiescin Q6 (QSOX1), a flavin-dependent sulfhydryl oxidase that catalyzes disulfide bond formation during protein maturation and extracellular matrix (ECM) remodeling. The enzyme functions within secretory pathway and extracellular compartments to promote oxidative folding and stabilization of proteins, influencing cell adhesion, migration, and redox homeostasis. QSOX1 activity intersects with proteostasis and ECM-associated signaling processes that shape tissue architecture and cellular stress responses. Altered QSOX1 expression has been reported in contexts relevant to fibrosis, tumor microenvironment remodeling, and inflammatory tissue remodeling, making it a useful target for mechanistic studies of redox-regulated ECM dynamics.
quiescin Q6 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the QSOX1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within QSOX1. 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 QSOX1 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 QSOX1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.