SLITRK5 Double Nickase Plasmid (h): sc-411868-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SLITRK5 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
- SLITRK5 Double Nickase Plasmid (h) and SLITRK5 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLITRK5. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SLITRK5 Double Nickase Plasmid (h) | sc-411868-NIC | 20 µg | $410.00 | |||
SLITRK5 Double Nickase Plasmid (h2) | sc-411868-NIC-2 | 20 µg | $410.00 |
SLITRK5 encodes a neuronal transmembrane protein of the SLITRK family implicated in neurite outgrowth, synapse development, and the organization of excitatory synaptic connections. Through its extracellular leucine-rich repeat domains, SLITRK5 participates in cell–cell recognition and signaling events that shape synaptic maturation and circuit refinement during neurodevelopment. Altered SLITRK5 expression or function has been associated with neuropsychiatric and neurodevelopmental phenotypes, including obsessive–compulsive disorder–related traits and changes in cortico-striatal circuitry. As a result, SLITRK5 is frequently studied in pathways governing synaptogenesis, neurite patterning, and activity-dependent neuronal connectivity.
SLITRK5 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLITRK5 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SLITRK5. 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 SLITRK5 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 SLITRK5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.