SLC35B4 Double Nickase Plasmid (h): sc-413728-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SLC35B4 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
- SLC35B4 Double Nickase Plasmid (h) and SLC35B4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLC35B4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SLC35B4 Double Nickase Plasmid (h) | sc-413728-NIC | 20 µg | $410.00 | |||
SLC35B4 Double Nickase Plasmid (h2) | sc-413728-NIC-2 | 20 µg | $410.00 |
SLC35B4 encodes a Golgi-localized nucleotide sugar transporter that imports UDP-xylose and UDP-N-acetylglucosamine into the Golgi lumen to support glycosylation and proteoglycan biosynthesis. By regulating nucleotide-sugar availability, SLC35B4 influences the composition and maturation of glycans on secreted and membrane proteins, affecting cell-surface signaling and protein trafficking. Altered nucleotide-sugar transport and downstream glycosylation patterns have been linked to changes in metabolic regulation, cell growth, and stress responses, making SLC35B4 a relevant node for studying glycan-dependent pathways. Dysregulated glycosylation is frequently associated with complex disease biology, including metabolic dysfunction and oncogenic phenotypes, providing a mechanistic context for research models.
SLC35B4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLC35B4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SLC35B4. 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 SLC35B4 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 SLC35B4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.