Slit3 Double Nickase Plasmid (h): sc-402553-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Slit3 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
- Slit3 Double Nickase Plasmid (h) and Slit3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLIT3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Slit3 Antibody (3C5): sc-293463
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Slit3 Double Nickase Plasmid (h) | sc-402553-NIC | 20 µg | $410.00 | |||
Slit3 Double Nickase Plasmid (h2) | sc-402553-NIC-2 | 20 µg | $410.00 |
SLIT3 encodes Slit3, a secreted guidance cue that signals primarily through ROBO receptors to regulate axon pathfinding, neuronal migration, and tissue patterning. In addition to nervous system development, SLIT3 contributes to cell–cell communication influencing cytoskeletal dynamics, directional motility, and vascular and connective tissue organization. Slit/ROBO signaling intersects with Rho GTPase and focal adhesion–related processes that shape adhesion and migration programs in multiple cell types. Dysregulated SLIT3 expression or pathway activity has been associated with altered developmental phenotypes and has been investigated in contexts involving aberrant cell migration and tumor biology.
Slit3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLIT3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SLIT3. 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 SLIT3 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 SLIT3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.