Gα q Double Nickase Plasmid (h): sc-400500-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Gα q 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 q Double Nickase Plasmid (h) and Gα q Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GNAQ. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Gα q Antibody (10): sc-136181
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Gα q Double Nickase Plasmid (h) | sc-400500-NIC | 20 µg | $410.00 | |||
Gα q Double Nickase Plasmid (h2) | sc-400500-NIC-2 | 20 µg | $410.00 |
GNAQ encodes the heterotrimeric G protein alpha subunit Gαq, a central transducer of signals from G protein–coupled receptors to phospholipase C-β. Upon activation, Gαq promotes PIP2 hydrolysis to generate IP3 and DAG, elevating intracellular Ca2+ and activating PKC, thereby impacting MAPK signaling, cytoskeletal dynamics, secretion, and transcriptional programs. GNAQ-dependent signaling shapes cell fate decisions in multiple tissues and is frequently examined in the context of aberrant GPCR-driven growth and survival pathways. Recurrent activating alterations in GNAQ are associated with melanocytic neoplasia biology and other disorders where dysregulated calcium/PKC–MAPK signaling contributes to pathogenic phenotypes.
Gα q Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GNAQ locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GNAQ. 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 GNAQ 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 GNAQ-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.