GABAA Rπ Double Nickase Plasmid (h): sc-404623-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GABAA Rπ 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
- GABAA Rπ Double Nickase Plasmid (h) and GABAA Rπ Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GABRP. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GABAA Rπ Double Nickase Plasmid (h) | sc-404623-NIC | 20 µg | $410.00 | |||
GABAA Rπ Double Nickase Plasmid (h2) | sc-404623-NIC-2 | 20 µg | $410.00 |
GABRP encodes the π subunit of the human GABA\(_A\) receptor, a ligand-gated chloride channel that mediates inhibitory neurotransmission and shapes membrane excitability through fast synaptic and extrasynaptic signaling. Incorporation of the π subunit can alter receptor assembly, gating kinetics, and pharmacology, influencing chloride flux, neuronal firing patterns, and broader circuit-level inhibition. GABA\(_A\) receptor signaling interfaces with processes such as synaptic plasticity, neurodevelopment, and stress-responsive modulation of neuronal networks. Dysregulated GABAergic signaling, including altered receptor subunit composition, has been associated in the literature with neurological and neuropsychiatric phenotypes, supporting investigation of GABRP in disease-relevant cellular models.
GABAA Rπ Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GABRP locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GABRP. 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 GABRP 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 GABRP-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.