DSCAM Double Nickase Plasmid (h): sc-403385-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DSCAM 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
- DSCAM Double Nickase Plasmid (h) and DSCAM Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DSCAM. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DSCAM Double Nickase Plasmid (h) | sc-403385-NIC | 20 µg | $410.00 | |||
DSCAM Double Nickase Plasmid (h2) | sc-403385-NIC-2 | 20 µg | $410.00 |
DSCAM (Down syndrome cell adhesion molecule) is an immunoglobulin superfamily receptor that mediates cell–cell recognition and adhesion during neurodevelopment. In human neurons, DSCAM supports neurite outgrowth, axon guidance, dendritic arborization, and synaptic organization by coordinating contact-dependent signaling and cytoskeletal dynamics. Through its extracellular binding and intracellular signaling interfaces, DSCAM contributes to pathways governing neuronal wiring specificity and circuit assembly. Dysregulated DSCAM dosage or function has been associated with neurodevelopmental phenotypes, including features linked to Down syndrome and autism spectrum-related synaptic and connectivity alterations.
DSCAM Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DSCAM locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DSCAM. 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 DSCAM 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 DSCAM-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.