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 β3/ITGB3/CD61 Double Nickase Plasmid (m): sc-421175-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Integrin β3/ITGB3/CD61 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
- Integrin β3/ITGB3/CD61 Double Nickase Plasmid (m) and Integrin β3/ITGB3/CD61 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Itgb3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Integrin β3/ITGB3/CD61 Antibody (D-11): sc-365679
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Integrin β3/ITGB3/CD61 Double Nickase Plasmid (m) | sc-421175-NIC | 20 µg | $410.00 | |||
Integrin β3/ITGB3/CD61 Double Nickase Plasmid (m2) | sc-421175-NIC-2 | 20 µg | $410.00 |
Mouse Itgb3 encodes integrin β3 (ITGB3/CD61), a transmembrane adhesion receptor that pairs with αIIb or αV to form heterodimeric integrins central to platelet aggregation, cell–matrix adhesion, and outside-in/inside-out signaling. ITGB3 regulates focal adhesion dynamics and cytoskeletal remodeling through pathways including FAK/Src, PI3K–AKT, and Rho-family GTPases, coordinating migration, survival, and mechanotransduction. In immune and stromal contexts, ITGB3-mediated interactions with extracellular matrix ligands influence inflammatory trafficking and tissue remodeling, while altered integrin signaling has been linked to hemostatic dysfunction and aberrant vascular and tumor-associated microenvironment phenotypes in experimental models. These properties make Itgb3 a valuable target for studying integrin-dependent signaling networks, adhesion-dependent gene regulation, and context-specific responses to biomechanical cues.
Integrin β3/ITGB3/CD61 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Itgb3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Itgb3. 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 Itgb3 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 Itgb3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.