GIPR Double Nickase Plasmid (h): sc-402895-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GIPR 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
- GIPR Double Nickase Plasmid (h) and GIPR Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GIPR. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GIPR Double Nickase Plasmid (h) | sc-402895-NIC | 20 µg | $410.00 | |||
GIPR Double Nickase Plasmid (h2) | sc-402895-NIC-2 | 20 µg | $410.00 |
GIPR encodes the glucose-dependent insulinotropic polypeptide receptor, a class B GPCR predominantly coupled to Gs that elevates intracellular cAMP and activates PKA and downstream CREB-mediated transcription. In pancreatic β cells and other metabolic tissues, GIPR integrates nutrient-induced incretin signaling to modulate insulin secretion, lipid handling, and energy balance, with pathway crosstalk to ERK/MAPK and PI3K signaling depending on cellular context. Altered GIPR expression or signaling dynamics have been linked to metabolic phenotypes including obesity and dysglycemia, and the receptor is also studied for roles in adipocyte biology and islet adaptation under metabolic stress.
GIPR Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GIPR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GIPR. 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 GIPR 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 GIPR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.