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.
IGF-1 Receptor α/β/IGF1R Double Nickase Plasmid (h): sc-400084-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IGF-1 Receptor α/β/IGF1R 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
- IGF-1 Receptor α/β/IGF1R Double Nickase Plasmid (h) and IGF-1 Receptor α/β/IGF1R Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IGF1R. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: IGF-1 Receptor/IGF1R Antibody (7G11): sc-81464
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IGF-1 Receptor α/β/IGF1R Double Nickase Plasmid (h) | sc-400084-NIC | 20 µg | $410.00 | |||
IGF-1 Receptor α/β/IGF1R Double Nickase Plasmid (h2) | sc-400084-NIC-2 | 20 µg | $410.00 |
IGF1R encodes the insulin-like growth factor 1 receptor, a disulfide-linked α/β receptor tyrosine kinase that transduces IGF signals to regulate proliferation, survival, metabolism, and differentiation. Ligand binding promotes receptor autophosphorylation and engages IRS/SHC adaptor proteins to activate PI3K–AKT–mTOR and RAS–RAF–MEK–ERK signaling, coordinating cell-cycle progression and anti-apoptotic responses. IGF1R activity intersects with integrin signaling and feedback regulation of insulin/IGF pathways, influencing cellular stress responses and anabolic growth programs. Dysregulated IGF1R signaling is associated with oncogenic transformation, therapy resistance mechanisms, and altered growth control in multiple disease contexts, supporting its utility as a pathway node in mechanistic studies.
IGF-1 Receptor α/β/IGF1R Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IGF1R locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IGF1R. 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 IGF1R 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 IGF1R-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.