FAK Double Nickase Plasmid (m): sc-420280-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FAK 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
- FAK Double Nickase Plasmid (m) and FAK Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ptk2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: FAK Antibody (D-1): sc-271126
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FAK Double Nickase Plasmid (m) | sc-420280-NIC | 20 µg | $410.00 | |||
FAK Double Nickase Plasmid (m2) | sc-420280-NIC-2 | 20 µg | $410.00 |
Mouse Ptk2 encodes focal adhesion kinase (FAK), a non-receptor tyrosine kinase that integrates integrin and growth factor signaling to coordinate focal adhesion turnover, actin cytoskeleton remodeling, and mechanotransduction. FAK phosphorylation-dependent scaffolding functions couple extracellular matrix engagement to downstream pathways including PI3K–AKT, MAPK/ERK, and Rho-family GTPase signaling, thereby regulating cell migration, survival, and proliferation. In vivo and cellular models link altered FAK activity to aberrant adhesion dynamics, invasive behavior, and fibro-inflammatory remodeling, making Ptk2 a key node in studies of tumor microenvironment interactions and tissue homeostasis.
FAK Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ptk2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ptk2. 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 Ptk2 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 Ptk2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.