DSCD75 Double Nickase Plasmid (h): sc-412188-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DSCD75 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
- DSCD75 Double Nickase Plasmid (h) and DSCD75 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting THEM6. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: DSCD75 Antibody (A-8): sc-374256
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DSCD75 Double Nickase Plasmid (h) | sc-412188-NIC | 20 µg | $410.00 | |||
DSCD75 Double Nickase Plasmid (h2) | sc-412188-NIC-2 | 20 µg | $410.00 |
Human THEM6 encodes DSCD75, an endoplasmic reticulum–associated transmembrane protein implicated in lipid metabolic processes and maintenance of membrane homeostasis. THEM6 has been linked to regulation of fatty acid handling and ER function, connecting it to pathways that coordinate lipid biosynthesis, organelle membrane composition, and cellular stress responses. Perturbation of these processes is relevant to phenotypes involving altered lipid signaling and metabolic adaptation, which are frequently studied in proliferative and stress-conditioned cell states. As a result, DSCD75 is commonly investigated in the context of ER–lipid network remodeling and downstream effects on cellular physiology.
DSCD75 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the THEM6 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within THEM6. 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 THEM6 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 THEM6-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.