FJX1 Double Nickase Plasmid (m): sc-420360-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FJX1 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
- FJX1 Double Nickase Plasmid (m) and FJX1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Fjx1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FJX1 Double Nickase Plasmid (m) | sc-420360-NIC | 20 µg | $410.00 |
Mouse Fjx1 encodes four-jointed box 1 (FJX1), a conserved Golgi-associated protein implicated in regulation of planar cell polarity and tissue morphogenesis. FJX1 is linked to pathways controlling growth and pattern formation, including modulation of Hippo signaling outputs and crosstalk with Wnt/PCP-related processes that influence cell proliferation and directional organization. During development, Fjx1 contributes to coordinated epithelial behavior and organ shaping, making it relevant for studying differentiation programs and morphogenetic control. Dysregulated FJX1 expression has been associated with altered growth control and migratory phenotypes in disease contexts, supporting its utility as a mechanistic node in signaling and tissue architecture studies.
FJX1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Fjx1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Fjx1. 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 Fjx1 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 Fjx1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.