REDD-1 Double Nickase Plasmid (r): sc-437314-NIC
- Target species: rat
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- REDD-1 Double Nickase Plasmid (r) 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
- REDD-1 Double Nickase Plasmid (r) and REDD-1 Double Nickase Plasmid (r2) encode distinct paired gRNA designs targeting . One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
REDD-1 Double Nickase Plasmid (r) | sc-437314-NIC | 20 µg | $410.00 | |||
REDD-1 Double Nickase Plasmid (r2) | sc-437314-NIC-2 | 20 µg | $410.00 |
REDD-1 (also known as DDIT4) is a stress-inducible regulator that links hypoxia, DNA damage, oxidative stress, and nutrient limitation to suppression of mTORC1 signaling through the TSC1/2–Rheb axis. In rat cells, REDD-1 helps coordinate metabolic adaptation by limiting protein synthesis and cell growth while influencing autophagy, mitochondrial function, and redox homeostasis. Altered REDD-1 expression has been associated with dysregulated mTOR activity and stress tolerance phenotypes relevant to metabolic dysfunction, ischemia-related injury models, and inflammation-associated tissue remodeling. Because REDD-1 sits at a convergence point of HIF-1, AMPK, and mTOR pathways, it is frequently used to interrogate stress-response circuitry and downstream transcriptional and proteostatic programs.
REDD-1 Double Nickase Plasmid (r) consists of a matched pair of plasmids engineered for high-specificity editing of the locus in rat cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within . 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 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 -disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.