FucT-VII Double Nickase Plasmid (h): sc-408027-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FucT-VII 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
- FucT-VII Double Nickase Plasmid (h) and FucT-VII Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FUT7. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FucT-VII Double Nickase Plasmid (h) | sc-408027-NIC | 20 µg | $410.00 | |||
FucT-VII Double Nickase Plasmid (h2) | sc-408027-NIC-2 | 20 µg | $410.00 |
FUT7 encodes α1,3-fucosyltransferase VII (FucT-VII), a Golgi-localized glycosyltransferase that catalyzes terminal fucosylation steps required for synthesis of sialyl Lewis X and related fucosylated glycans. This activity is central to leukocyte adhesion biology by enabling functional selectin ligands on glycoproteins and glycolipids, supporting leukocyte rolling and trafficking during inflammation. FUT7-mediated glycosylation intersects with broader glycan biosynthesis pathways that shape cell–cell recognition, receptor signaling, and immune-cell surface architecture. Altered FUT7 expression or fucosylation patterns have been associated with dysregulated inflammatory responses and tumor-associated glycan remodeling, making it a useful target for mechanistic studies of adhesion and glyco-immune interactions.
FucT-VII Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FUT7 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FUT7. 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 FUT7 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 FUT7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.