β-1,3-Gal-T4 Double Nickase Plasmid (m): sc-424825-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- β-1,3-Gal-T4 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
- β-1,3-Gal-T4 Double Nickase Plasmid (m) and β-1,3-Gal-T4 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting B3galt4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
β-1,3-Gal-T4 Double Nickase Plasmid (m) | sc-424825-NIC | 20 µg | $410.00 |
Mouse B3galt4 encodes β-1,3-Gal-T4, a Golgi-localized glycosyltransferase that catalyzes β1,3-galactosylation steps important for glycolipid and glycoprotein biosynthesis. Through its role in assembling complex glycans, B3galt4 contributes to membrane microdomain organization, receptor trafficking, and cell–cell communication processes that intersect with glycosphingolipid metabolism and broader glycosylation pathways. Altered glycosylation patterns are frequently linked to changes in neuronal function, immune signaling, and tumor cell phenotypes, making B3galt4 a relevant node for studying glycome-dependent regulation. B3galt4 perturbation is therefore useful for probing how specific glycan structures modulate signaling and adhesion in developmental and disease-relevant cellular contexts.
β-1,3-Gal-T4 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the B3galt4 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within B3galt4. 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 B3galt4 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 B3galt4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.