Gα olf Double Nickase Plasmid (h): sc-401092-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Gα olf 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
- Gα olf Double Nickase Plasmid (h) and Gα olf Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GNAL. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Gα olf Double Nickase Plasmid (h) | sc-401092-NIC | 20 µg | $410.00 | |||
Gα olf Double Nickase Plasmid (h2) | sc-401092-NIC-2 | 20 µg | $410.00 |
GNAL encodes the human olfactory G protein alpha subunit Gαolf, a heterotrimeric Gα that couples select G protein–coupled receptors to adenylyl cyclase activation and cAMP production. Beyond sensory signaling, Gαolf is a key transducer in striatal neurons, integrating dopaminergic and adenosinergic inputs to regulate PKA-dependent phosphorylation programs and transcriptional responses. This signaling axis shapes neuronal excitability and synaptic plasticity through downstream effectors including CREB and ion channel modulation. Genetic and functional perturbations of GNAL have been linked to movement-disorder phenotypes, supporting its relevance for studying GPCR–cAMP pathway dysregulation in neurobiology.
Gα olf Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GNAL locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GNAL. 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 GNAL 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 GNAL-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.