Glucagon Receptor Double Nickase Plasmid (h): sc-402018-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Glucagon Receptor 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
- Glucagon Receptor Double Nickase Plasmid (h) and Glucagon Receptor Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GCGR. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Glucagon Receptor Double Nickase Plasmid (h) | sc-402018-NIC | 20 µg | $410.00 | |||
Glucagon Receptor Double Nickase Plasmid (h2) | sc-402018-NIC-2 | 20 µg | $410.00 |
Human GCGR encodes the glucagon receptor, a class B G protein–coupled receptor that governs hepatic glucose output and whole-body energy balance in response to glucagon. Upon ligand binding, GCGR primarily couples to Gs to elevate cAMP and activate PKA, integrating with CREB-dependent transcriptional programs that regulate gluconeogenesis, glycogenolysis, and lipid metabolism. GCGR signaling intersects with insulin–glucagon counterregulation, nutrient sensing, and endocrine control of metabolic homeostasis. Dysregulated GCGR pathway activity is implicated in metabolic disease–relevant phenotypes, including altered glycemic control, hepatic lipid handling, and endocrine pancreas–liver axis dysfunction.
Glucagon Receptor Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GCGR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GCGR. 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 GCGR 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 GCGR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.