leupaxin Double Nickase Plasmid (m): sc-430706-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- leupaxin 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
- leupaxin Double Nickase Plasmid (m) and leupaxin Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Lpxn. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
leupaxin Double Nickase Plasmid (m) | sc-430706-NIC | 20 µg | $410.00 | |||
leupaxin Double Nickase Plasmid (m2) | sc-430706-NIC-2 | 20 µg | $410.00 |
Mouse Lpxn encodes leupaxin, a paxillin family focal adhesion adaptor that coordinates integrin-dependent signaling and actin cytoskeletal remodeling. Leupaxin localizes to adhesion complexes and interfaces with kinases and scaffolding proteins to influence cell spreading, migration, and mechanotransduction, integrating cues from the extracellular matrix into downstream pathways such as focal adhesion signaling and Rho GTPase-regulated dynamics. In immune and stromal contexts, altered leupaxin activity can modulate adhesion-dependent activation states and tissue remodeling programs, making Lpxn a useful node for studying inflammatory microenvironments and cell motility phenotypes relevant to cancer biology and vascular or fibrotic remodeling.
leupaxin Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Lpxn locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Lpxn. 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 Lpxn 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 Lpxn-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.