IGFBP4 Double Nickase Plasmid (m): sc-421065-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IGFBP4 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
- IGFBP4 Double Nickase Plasmid (m) and IGFBP4 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Igfbp4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IGFBP4 Double Nickase Plasmid (m) | sc-421065-NIC | 20 µg | $410.00 |
Igfbp4 encodes insulin-like growth factor binding protein 4 (IGFBP4), a secreted regulator of IGF bioavailability that modulates IGF1/IGF2 interactions with IGF receptors and influences downstream PI3K–AKT and MAPK signaling. By sequestering IGFs and shaping local growth factor gradients, IGFBP4 contributes to control of cell proliferation, differentiation, survival, and tissue remodeling. In mouse biology, Igfbp4 is studied in contexts such as vascular and cardiac homeostasis, skeletal development, and reproductive and metabolic regulation, where IGF signaling is a key driver of phenotypic outcomes. Dysregulated IGFBP4/IGF axis activity has been associated with disease-relevant processes including fibrosis, angiogenesis, and aberrant growth control, making Igfbp4 a useful locus for mechanistic pathway studies.
IGFBP4 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Igfbp4 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Igfbp4. 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 Igfbp4 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 Igfbp4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.