SESN3 Double Nickase Plasmid (m): sc-429191-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SESN3 Double Nickase Plasmid (m) 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
- SESN3 Double Nickase Plasmid (m) and SESN3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Sesn3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SESN3 Double Nickase Plasmid (m) | sc-429191-NIC | 20 µg | $410.00 |
Sesn3 encodes Sestrin 3 (SESN3), a stress-inducible protein that helps coordinate cellular adaptation to metabolic and oxidative challenges. In mouse cells, SESN3 is linked to nutrient-sensing and redox homeostasis programs, interfacing with AMPK–mTOR signaling and broader autophagy and antioxidant response networks. Through these pathways, SESN3 can influence mitochondrial function, proteostasis, and inflammatory signaling, making it relevant to studies of metabolic dysregulation and tissue stress responses. Altered SESN3 activity has been investigated in the context of obesity-related phenotypes, insulin signaling changes, and inflammatory states, supporting its use as a node for mechanistic pathway interrogation.
SESN3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Sesn3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Sesn3. 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 Sesn3 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 Sesn3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.