Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
INSR/Insulin Receptor Double Nickase Plasmid (h): sc-400075-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- INSR/Insulin 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
- INSR/Insulin Receptor Double Nickase Plasmid (h) and INSR/Insulin Receptor Double Nickase Plasmid (h2) 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 (h) | sc-400075-NIC | 20 µg | $410.00 | |||
INSR/Insulin Receptor Double Nickase Plasmid (h2) | sc-400075-NIC-2 | 20 µg | $410.00 |
INSR encodes the human insulin receptor, a receptor tyrosine kinase that initiates insulin-dependent signaling to regulate glucose uptake, glycogen and lipid metabolism, and cell growth. Upon ligand binding and autophosphorylation, INSR recruits adaptor proteins such as IRS1/2 to activate PI3K–AKT–mTOR and RAS–RAF–MEK–ERK pathways, coordinating metabolic and mitogenic programs. INSR function influences vesicular trafficking of GLUT4 and broader control of nutrient sensing and anabolic signaling. Dysregulated INSR signaling is implicated in insulin resistance and metabolic disease and is also leveraged by many tumor types to support proliferation and survival phenotypes.
INSR/Insulin Receptor Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the INSR locus in human 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.