α-parvin Double Nickase Plasmid (h): sc-405769-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- α-parvin 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
- α-parvin Double Nickase Plasmid (h) and α-parvin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PARVA. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
α-parvin Double Nickase Plasmid (h) | sc-405769-NIC | 20 µg | $410.00 |
PARVA encodes α-parvin, an actin-binding focal adhesion protein that associates with integrin-linked kinase (ILK) and PINCH to form the IPP complex, coupling integrin signaling to cytoskeletal remodeling. Through interactions with paxillin, actin, and focal adhesion components, α-parvin regulates cell adhesion, spreading, migration, and mechanotransduction, influencing pathways that control cell shape and tissue organization. PARVA-dependent adhesion dynamics are relevant to processes such as angiogenesis and extracellular matrix sensing, and altered expression or regulation has been linked in the literature to cancer cell invasion and metastasis-associated phenotypes. As a cytoskeletal adaptor at adhesion sites, α-parvin provides a useful entry point for studying integrin-mediated signaling and actin architecture in human cells.
α-parvin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PARVA locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PARVA. 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 PARVA 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 PARVA-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.