GABAA Rα3 Double Nickase Plasmid (h): sc-403044-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GABAA Rα3 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 Rα3 Double Nickase Plasmid (h) and GABAA Rα3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GABRA3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GABAA Rα3 Double Nickase Plasmid (h) | sc-403044-NIC | 20 µg | $410.00 | |||
GABAA Rα3 Double Nickase Plasmid (h2) | sc-403044-NIC-2 | 20 µg | $410.00 |
GABRA3 encodes the human γ-aminobutyric acid type A receptor α3 subunit (GABAA Rα3), a ligand-gated chloride channel component that mediates fast inhibitory neurotransmission in the central nervous system. Incorporation of α3 into pentameric GABAA receptors influences channel kinetics, synaptic versus extrasynaptic signaling, and neuronal excitability through chloride conductance and membrane potential regulation. GABAergic signaling via GABAA receptors integrates with phosphorylation-dependent modulation, receptor trafficking, and synapse organization pathways that shape network oscillations and developmental circuit formation. Altered expression or function of GABAA receptor subunits, including GABRA3, is studied in the context of neurodevelopmental and neuropsychiatric phenotypes and seizure-related mechanisms.
GABAA Rα3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GABRA3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GABRA3. 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 GABRA3 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 GABRA3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.