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 α2/ITGA2/CD49b Double Nickase Plasmid (h): sc-400913-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Integrin α2/ITGA2/CD49b 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 α2/ITGA2/CD49b Double Nickase Plasmid (h) and Integrin α2/ITGA2/CD49b Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ITGA2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Integrin α2/ITGA2/CD49b Antibody (C-9): sc-74466
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Integrin α2/ITGA2/CD49b Double Nickase Plasmid (h) | sc-400913-NIC | 20 µg | $410.00 | |||
Integrin α2/ITGA2/CD49b Double Nickase Plasmid (h2) | sc-400913-NIC-2 | 20 µg | $410.00 |
ITGA2 encodes integrin α2 (CD49b), which heterodimerizes with integrin β1 to form the α2β1 collagen/laminin receptor that mediates cell–extracellular matrix adhesion and mechanotransduction. Through coupling to focal adhesion kinase signaling, Src-family kinases, and Rho GTPase–dependent cytoskeletal remodeling, ITGA2 influences cell migration, invasion, and survival responses to matrix composition and stiffness. In platelets and other cell types, α2β1 supports collagen-dependent adhesion and integrin “outside-in” signaling that can modulate activation states. Dysregulated ITGA2 expression or integrin signaling is frequently studied in the context of tumor–stroma interactions, fibrotic remodeling, inflammatory cell trafficking, and thrombosis-associated phenotypes.
Integrin α2/ITGA2/CD49b Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ITGA2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ITGA2. 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 ITGA2 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 ITGA2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.