Date published: 2026-7-9

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β-1,4-Gal-T4 Double Nickase Plasmid (h): sc-407251-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • β-1,4-Gal-T4 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
  • β-1,4-Gal-T4 Double Nickase Plasmid (h) and β-1,4-Gal-T4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting B4GALT4. One or both designs may be available
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    β-1,4-Gal-T4 Double Nickase Plasmid (h)

    sc-407251-NIC
    20 µg
    $410.00

    B4GALT4 encodes human β-1,4-galactosyltransferase 4 (β-1,4-Gal-T4), a Golgi-resident glycosyltransferase that transfers galactose to N-acetylglucosamine to generate β1,4-linked galactosylated glycans on glycoproteins and glycolipids. Through its contribution to N-glycan processing and lactosamine extension, β-1,4-Gal-T4 influences glycan-dependent protein trafficking, receptor organization at the cell surface, and lectin-mediated cell–cell interactions. Altered β1,4-galactosylation is frequently studied in the context of dysregulated glycosylation programs that shape signaling, adhesion, and immune recognition in disease-associated cellular states. B4GALT4 is therefore relevant to mechanistic investigations of Golgi glycosylation pathways and how glycan remodeling affects cellular phenotype.

    β-1,4-Gal-T4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the B4GALT4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within B4GALT4. 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 B4GALT4 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 B4GALT4-disrupted clones.

    For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.