PSD-93 Double Nickase Plasmid (h): sc-405011-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PSD-93 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
- PSD-93 Double Nickase Plasmid (h) and PSD-93 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DLG2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PSD-93 Double Nickase Plasmid (h) | sc-405011-NIC | 20 µg | $410.00 | |||
PSD-93 Double Nickase Plasmid (h2) | sc-405011-NIC-2 | 20 µg | $410.00 |
DLG2 encodes postsynaptic density protein 93 (PSD-93), a MAGUK family scaffold enriched at excitatory synapses where it organizes glutamatergic receptor complexes and couples them to downstream signaling. PSD-93 contains PDZ, SH3, and GK domains that coordinate trafficking and stabilization of NMDA/AMPA receptor-associated proteins, shaping synaptic strength and activity-dependent plasticity. Through interactions within the postsynaptic density, DLG2 influences synapse maturation, neuronal connectivity, and signal transduction pathways that govern learning-related circuit function. Genetic and functional studies have linked altered DLG2 expression or variation to neurodevelopmental and neuropsychiatric phenotypes, supporting its use as a molecular entry point for dissecting synaptic dysfunction mechanisms.
PSD-93 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DLG2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DLG2. 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 DLG2 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 DLG2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.