SLC35D1 Double Nickase Plasmid (h): sc-407065-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SLC35D1 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
- SLC35D1 Double Nickase Plasmid (h) and SLC35D1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLC35D1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SLC35D1 Double Nickase Plasmid (h) | sc-407065-NIC | 20 µg | $410.00 | |||
SLC35D1 Double Nickase Plasmid (h2) | sc-407065-NIC-2 | 20 µg | $410.00 |
SLC35D1 encodes a Golgi-resident nucleotide sugar transporter that exchanges UDP-sugars across intracellular membranes to support glycosaminoglycan and proteoglycan biosynthesis. By regulating the luminal availability of substrates for glycosyltransferases, SLC35D1 influences extracellular matrix assembly and cartilage-related developmental processes. Altered SLC35D1 function has been linked to defects in chondrogenesis and skeletal morphogenesis, consistent with its role in proteoglycan-rich matrix formation. In cell models, perturbation of SLC35D1 can be used to interrogate how nucleotide sugar flux controls glycosylation-dependent signaling and matrix-dependent phenotypes.
SLC35D1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLC35D1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SLC35D1. 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 SLC35D1 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 SLC35D1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.