GCNT1 Double Nickase Plasmid (h): sc-410791-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GCNT1 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
- GCNT1 Double Nickase Plasmid (h) and GCNT1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GCNT1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GCNT1 Double Nickase Plasmid (h) | sc-410791-NIC | 20 µg | $410.00 | |||
GCNT1 Double Nickase Plasmid (h2) | sc-410791-NIC-2 | 20 µg | $410.00 |
GCNT1 encodes a Golgi-resident glycosyltransferase that catalyzes formation of core 2 and related branched O-glycans by transferring N-acetylglucosamine to Galβ1-3GalNAc structures on glycoproteins. By remodeling mucin-type O-glycosylation, GCNT1 influences lectin binding, receptor trafficking, and cell–cell adhesion processes that shape immune cell interactions and epithelial barrier properties. Altered GCNT1 activity can shift cell-surface glycan motifs, affecting selectin ligand presentation and downstream inflammatory signaling. Dysregulated O-glycan branching associated with GCNT1 has been reported in contexts of immune dysfunction and malignant transformation, supporting its study in glycoimmunology and cancer cell biology.
GCNT1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GCNT1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GCNT1. 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 GCNT1 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 GCNT1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.