β3Gn-T3 Double Nickase Plasmid (m): sc-428303-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- β3Gn-T3 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
- β3Gn-T3 Double Nickase Plasmid (m) and β3Gn-T3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting B3gnt3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
β3Gn-T3 Double Nickase Plasmid (m) | sc-428303-NIC | 20 µg | $410.00 | |||
β3Gn-T3 Double Nickase Plasmid (m2) | sc-428303-NIC-2 | 20 µg | $410.00 |
B3gnt3 encodes β3Gn-T3, a β-1,3-N-acetylglucosaminyltransferase that contributes to extension of poly-N-acetyllactosamine on glycoproteins and glycolipids within the Golgi. By shaping N- and O-glycan branching and terminal structures, β3Gn-T3 influences lectin-mediated interactions, cell–cell adhesion, and receptor trafficking that impact immune and epithelial biology. Altered glycosyltransferase activity can remodel the cell-surface glycome, affecting signaling thresholds and inflammatory cues relevant to models of infection, mucosal homeostasis, and tumor-associated glycosylation changes. In mouse systems, B3gnt3 perturbation is used to investigate how glycan elongation regulates ligand recognition and downstream pathway activation.
β3Gn-T3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the B3gnt3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within B3gnt3. 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 B3gnt3 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 B3gnt3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.