KY peptidase Double Nickase Plasmid (m): sc-421366-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KY peptidase Double Nickase Plasmid (m) 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
- KY peptidase Double Nickase Plasmid (m) and KY peptidase Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ky. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KY peptidase Double Nickase Plasmid (m) | sc-421366-NIC | 20 µg | $410.00 | |||
KY peptidase Double Nickase Plasmid (m2) | sc-421366-NIC-2 | 20 µg | $410.00 |
Ky encodes KY peptidase, a muscle-enriched protein implicated in maintaining skeletal muscle integrity and sarcomeric organization, with roles in proteostasis and structural remodeling during myofiber stress. In mouse, KY peptidase activity is linked to pathways governing myofibril maintenance and turnover, supporting normal contractile function and resistance to damage. Disruption of Ky has been associated with neuromuscular phenotypes consistent with muscular dystrophy–like pathology, making it a useful gene for studying myopathy mechanisms. KY peptidase is therefore relevant for research on muscle degeneration, regeneration, and protein quality control networks in striated tissue.
KY peptidase Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ky locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ky. 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 Ky 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 Ky-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.