INSR/Insulin Receptor Double Nickase Plasmid (m): sc-421142-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- INSR/Insulin Receptor 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
- INSR/Insulin Receptor Double Nickase Plasmid (m) and INSR/Insulin Receptor Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Insr. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: INSR/Insulin Receptor β Antibody (CT-3): sc-57342
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
INSR/Insulin Receptor Double Nickase Plasmid (m) | sc-421142-NIC | 20 µg | $410.00 | |||
INSR/Insulin Receptor Double Nickase Plasmid (m2) | sc-421142-NIC-2 | 20 µg | $410.00 |
Insr encodes the mouse insulin receptor (INSR), a receptor tyrosine kinase that binds insulin to initiate signaling through IRS adaptor proteins and downstream PI3K–AKT and RAS–MAPK cascades. These pathways coordinate glucose uptake, glycogen and lipid metabolism, protein synthesis, and cell survival, while also intersecting with nutrient-sensing networks such as mTOR. INSR activity influences insulin sensitivity in metabolic tissues including liver, muscle, and adipose, and it shapes cellular responses to hormonal and nutritional cues. Dysregulated Insr signaling is widely used as a mechanistic entry point for studying insulin resistance, metabolic homeostasis, and endocrine–metabolic phenotypes in mouse models and cell systems.
INSR/Insulin Receptor Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Insr locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Insr. 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 Insr 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 Insr-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.