SEMA7A Double Nickase Plasmid (m): sc-422890-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SEMA7A 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
- SEMA7A Double Nickase Plasmid (m) and SEMA7A Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Sema7a. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: SEMA7A Antibody (C-6): sc-374432
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SEMA7A Double Nickase Plasmid (m) | sc-422890-NIC | 20 µg | $410.00 |
Mouse Sema7a encodes semaphorin 7A (SEMA7A), a glycosylphosphatidylinositol-anchored guidance and immunomodulatory protein that regulates cell adhesion, migration, and neurite outgrowth. SEMA7A signals through integrins such as ITGA1/ITGB1 and can influence focal adhesion dynamics, MAPK pathways, and cytoskeletal remodeling, linking extracellular cues to directional movement and tissue patterning. In immune and stromal contexts, SEMA7A contributes to leukocyte trafficking and inflammatory signaling, and altered expression has been associated with neuroinflammation, fibrotic remodeling, and tumor microenvironment biology. These functions make Sema7a a useful target for dissecting pathways controlling axon guidance, immune cell activation, and microenvironment-driven cell motility in mouse models.
SEMA7A Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Sema7a locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Sema7a. 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 Sema7a 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 Sema7a-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.