DEPDC5 Double Nickase Plasmid (h): sc-402806-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DEPDC5 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
- DEPDC5 Double Nickase Plasmid (h) and DEPDC5 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DEPDC5. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DEPDC5 Double Nickase Plasmid (h) | sc-402806-NIC | 20 µg | $410.00 | |||
DEPDC5 Double Nickase Plasmid (h2) | sc-402806-NIC-2 | 20 µg | $410.00 |
DEPDC5 (DEP domain containing 5) encodes a core component of the GATOR1 complex, a negative regulator of mTORC1 signaling downstream of amino acid sensing at the lysosomal surface. By functioning as a GTPase-activating factor toward Rag GTPases, DEPDC5 helps restrain nutrient-driven mTORC1 activity, thereby influencing autophagy, protein synthesis, and cellular growth control. Disruption of DEPDC5 has been linked to dysregulated mTOR pathway signaling and altered neuronal excitability, with genetic associations reported in focal epilepsies and cortical malformations. These properties make DEPDC5 a useful target for mechanistic studies of mTORC1 regulation, metabolic signaling crosstalk, and neurodevelopmental pathway perturbation.
DEPDC5 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DEPDC5 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DEPDC5. 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 DEPDC5 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 DEPDC5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.