Lunapark Double Nickase Plasmid (h): sc-407336-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Lunapark 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
- Lunapark Double Nickase Plasmid (h) and Lunapark Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LNPK. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Lunapark Double Nickase Plasmid (h) | sc-407336-NIC | 20 µg | $410.00 |
Human LNPK encodes Lunapark, an endoplasmic reticulum (ER) membrane protein that localizes to three-way ER junctions and helps stabilize the tubular ER network. Lunapark functions in ER morphogenesis and maintenance of ER sheet–tubule balance, coordinating with membrane shaping factors to support organelle architecture, lipid handling, and intracellular signaling. Because ER structure is closely coupled to proteostasis, calcium homeostasis, and ER stress responses, perturbation of LNPK is relevant to studies of cell adaptation pathways that influence neuronal and secretory-cell vulnerability. Altered ER network dynamics have been associated with mechanisms implicated in neurodevelopmental and neurodegenerative phenotypes, making LNPK a useful target for dissecting ER organization-linked disease biology.
Lunapark Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LNPK locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LNPK. 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 LNPK 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 LNPK-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.