SEMA3C Double Nickase Plasmid (m): sc-422877-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SEMA3C 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
- SEMA3C Double Nickase Plasmid (m) and SEMA3C Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Sema3c. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SEMA3C Double Nickase Plasmid (m) | sc-422877-NIC | 20 µg | $410.00 | |||
SEMA3C Double Nickase Plasmid (m2) | sc-422877-NIC-2 | 20 µg | $410.00 |
Mouse Sema3c encodes SEMA3C, a secreted class 3 semaphorin that functions as a guidance cue regulating cytoskeletal remodeling, cell migration, and tissue patterning. SEMA3C signals primarily through neuropilin and plexin receptor complexes to modulate Rho family GTPases and downstream pathways that influence adhesion and directional movement. During development it contributes to axon pathfinding and cardiovascular morphogenesis, and dysregulated semaphorin signaling is frequently studied in contexts of abnormal vascular remodeling and invasive cell behavior. As a microenvironmental ligand, SEMA3C is also investigated for its roles in epithelial–mesenchymal transitions and intercellular communication in disease-relevant models.
SEMA3C Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Sema3c locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Sema3c. 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 Sema3c 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 Sema3c-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.