RETSAT Double Nickase Plasmid (h): sc-412368-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RETSAT 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
- RETSAT Double Nickase Plasmid (h) and RETSAT Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RETSAT. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RETSAT Double Nickase Plasmid (h) | sc-412368-NIC | 20 µg | $410.00 |
RETSAT (retinol saturase) encodes an oxidoreductase that catalyzes the saturation of all-trans-retinol to produce dihydroretinoids, shaping cellular retinoid pools and downstream transcriptional programs governed by retinoic acid signaling. By modulating retinoid metabolism, RETSAT influences processes linked to adipocyte differentiation, energy homeostasis, and cellular redox balance, and its activity intersects with lipid handling pathways that respond to nutritional and inflammatory cues. Altered RETSAT expression or retinoid flux has been reported in contexts of metabolic dysfunction and has been explored in relation to tumor biology, where retinoid-dependent differentiation and proliferation programs can be perturbed. These features make RETSAT a useful target for mechanistic studies of retinoid-driven gene regulation and lipid-associated phenotypes in human cell models.
RETSAT Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RETSAT locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RETSAT. 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 RETSAT 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 RETSAT-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.