Insulin II Double Nickase Plasmid (m): sc-421140-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Insulin II Double Nickase Plasmid (m) 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
- Insulin II Double Nickase Plasmid (m) and Insulin II Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ins2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Insulin II Double Nickase Plasmid (m) | sc-421140-NIC | 20 µg | $410.00 |
Mouse Ins2 encodes Insulin II, a pancreatic β-cell hormone central to glucose homeostasis and anabolic metabolism. Following glucose-stimulated secretion, insulin engages insulin receptor signaling to regulate PI3K–AKT and MAPK pathways, driving glucose uptake, glycogen synthesis, lipogenesis, and suppression of hepatic gluconeogenesis. Ins2 also influences β-cell function and survival through ER stress responses and proinsulin processing within the secretory pathway. Dysregulation of insulin production or signaling is tightly linked to metabolic disease phenotypes, making Ins2 a key target for mechanistic studies of glucose regulation and β-cell biology.
Insulin II Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ins2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ins2. 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 Ins2 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 Ins2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.