StARD7 Double Nickase Plasmid (h): sc-405820-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- StARD7 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
- StARD7 Double Nickase Plasmid (h) and StARD7 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting STARD7. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
StARD7 Double Nickase Plasmid (h) | sc-405820-NIC | 20 µg | $410.00 | |||
StARD7 Double Nickase Plasmid (h2) | sc-405820-NIC-2 | 20 µg | $410.00 |
STARD7 encodes the StAR-related lipid transfer domain protein 7 (StARD7), a lipid-transfer factor implicated in intracellular phospholipid trafficking and maintenance of mitochondrial membrane composition. By supporting mitochondrial homeostasis, StARD7 contributes to processes such as oxidative metabolism, membrane biogenesis, and cellular stress responses. Altered STARD7 expression or function has been associated with mitochondrial dysfunction phenotypes and has been studied in contexts including epithelial barrier regulation and inflammatory signaling. These features make STARD7 a useful target for interrogating lipid handling pathways that couple organelle integrity to cell physiology.
StARD7 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the STARD7 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within STARD7. 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 STARD7 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 STARD7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.