SEMA3C Double Nickase Plasmid (h): sc-402489-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SEMA3C 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
- SEMA3C Double Nickase Plasmid (h) and SEMA3C Double Nickase Plasmid (h2) 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 (h) | sc-402489-NIC | 20 µg | $410.00 | |||
SEMA3C Double Nickase Plasmid (h2) | sc-402489-NIC-2 | 20 µg | $410.00 |
SEMA3C encodes semaphorin-3C, a secreted guidance cue that signals through neuropilin and plexin receptors to regulate cytoskeletal remodeling, directional migration, and cell–cell interactions. In addition to roles in axon guidance and neural crest–related patterning, SEMA3C influences angiogenic and lymphatic remodeling and can modulate adhesive and invasive behavior through Rho family GTPase-dependent pathways. Dysregulated SEMA3C expression has been reported across multiple disease contexts, including tumor-associated remodeling and vascular pathology, making it a useful target for dissecting guidance signaling, microenvironment interactions, and migration phenotypes in human cell models.
SEMA3C Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SEMA3C locus in human 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.