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.
Integrin αV/ITGAV/CD51 Double Nickase Plasmid (h): sc-400506-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Integrin αV/ITGAV/CD51 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
- Integrin αV/ITGAV/CD51 Double Nickase Plasmid (h) and Integrin αV/ITGAV/CD51 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ITGAV. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Integrin αV/ITGAV/CD51 Antibody (P2W7): sc-9969
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Integrin αV/ITGAV/CD51 Double Nickase Plasmid (h) | sc-400506-NIC | 20 µg | $410.00 | |||
Integrin αV/ITGAV/CD51 Double Nickase Plasmid (h2) | sc-400506-NIC-2 | 20 µg | $410.00 |
ITGAV encodes integrin αV (CD51), an α subunit that pairs with multiple β integrins (e.g., β3, β5, β6, β8) to form receptors for extracellular matrix ligands containing RGD motifs such as vitronectin, fibronectin, and osteopontin. Through adhesion-dependent outside-in signaling, αV-containing integrins regulate focal adhesion dynamics, cytoskeletal remodeling, and cell migration via pathways including FAK/SRC, PI3K–AKT, and MAPK/ERK. ITGAV also contributes to mechanotransduction and can modulate TGF-β activation in the extracellular microenvironment through specific heterodimers, influencing epithelial–mesenchymal programs and tissue remodeling. Dysregulated αV integrin signaling is frequently investigated in contexts of tumor cell invasion, angiogenesis, fibrosis, and inflammatory cell trafficking, making ITGAV a common target in studies of adhesion and microenvironmental signaling.
Integrin αV/ITGAV/CD51 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ITGAV locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ITGAV. 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 ITGAV 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 ITGAV-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.