SLC35D2 Double Nickase Plasmid (h): sc-411557-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SLC35D2 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
- SLC35D2 Double Nickase Plasmid (h) and SLC35D2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLC35D2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SLC35D2 Double Nickase Plasmid (h) | sc-411557-NIC | 20 µg | $410.00 | |||
SLC35D2 Double Nickase Plasmid (h2) | sc-411557-NIC-2 | 20 µg | $410.00 |
SLC35D2 encodes a nucleotide sugar transporter localized to secretory pathway membranes, where it contributes to the import of activated sugar donors required for glycosylation reactions. By regulating the availability of nucleotide sugars in the endoplasmic reticulum and Golgi, SLC35D2 influences proteoglycan and glycoprotein biosynthesis that underpins extracellular matrix organization, receptor trafficking, and cell–cell communication. Perturbation of nucleotide sugar transport can remodel glycan structures and alter signaling outputs across developmentally and immunologically relevant pathways. Accordingly, SLC35D2 is studied in the context of congenital disorders of glycosylation and broader disease mechanisms where aberrant glycosylation impacts cellular homeostasis.
SLC35D2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLC35D2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SLC35D2. 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 SLC35D2 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 SLC35D2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.