UGT8 Double Nickase Plasmid (m): sc-423604-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- UGT8 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
- UGT8 Double Nickase Plasmid (m) and UGT8 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ugt8a. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
UGT8 Double Nickase Plasmid (m) | sc-423604-NIC | 20 µg | $410.00 |
Ugt8a encodes UDP-galactose:ceramide galactosyltransferase (UGT8), a Golgi-resident glycosyltransferase that catalyzes formation of galactosylceramide, a key sphingolipid enriched in myelinating glia. By controlling levels of galactosylceramide and related glycolipids, UGT8 influences membrane microdomain composition, vesicular trafficking, and myelin biogenesis, intersecting with broader sphingolipid metabolism and lipid homeostasis pathways. In mouse, altered UGT8 activity is relevant to studies of nervous system development and white matter integrity, and it provides a molecular entry point for investigating how glycolipid imbalance contributes to neuroinflammatory and neurodegenerative phenotypes in experimental models.
UGT8 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ugt8a locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ugt8a. 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 Ugt8a 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 Ugt8a-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.