ORMDL3 Double Nickase Plasmid (h): sc-403587-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ORMDL3 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
- ORMDL3 Double Nickase Plasmid (h) and ORMDL3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ORMDL3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ORMDL3 Double Nickase Plasmid (h) | sc-403587-NIC | 20 µg | $410.00 | |||
ORMDL3 Double Nickase Plasmid (h2) | sc-403587-NIC-2 | 20 µg | $410.00 |
ORMDL3 (orosomucoid-like 3) is an endoplasmic reticulum membrane protein that regulates sphingolipid biosynthesis by modulating serine palmitoyltransferase activity, thereby influencing ceramide homeostasis and lipid-mediated signaling. Through its role in ER lipid metabolism, ORMDL3 impacts ER stress responses, calcium handling, and inflammatory signaling pathways that shape cellular activation states. Altered ORMDL3 expression and associated lipid imbalances have been linked to immune dysregulation and airway inflammation phenotypes, making it a frequent target in studies of asthma susceptibility and related inflammatory traits. In human cell models, perturbing ORMDL3 provides a route to dissect how sphingolipid flux intersects with cytokine-driven programs, membrane composition, and stress-adaptive pathways.
ORMDL3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ORMDL3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ORMDL3. 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 ORMDL3 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 ORMDL3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.