ALG3 Double Nickase Plasmid (h): sc-411431-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ALG3 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
- ALG3 Double Nickase Plasmid (h) and ALG3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ALG3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ALG3 Double Nickase Plasmid (h) | sc-411431-NIC | 20 µg | $410.00 | |||
ALG3 Double Nickase Plasmid (h2) | sc-411431-NIC-2 | 20 µg | $410.00 |
ALG3 encodes an endoplasmic reticulum–localized α-1,3-mannosyltransferase that participates in the dolichol-linked oligosaccharide assembly pathway required for N-glycosylation. By catalyzing the addition of mannose residues during lipid-linked oligosaccharide biosynthesis, ALG3 supports proper folding, quality control, and trafficking of secretory and membrane proteins. Disruption of this step can alter glycoprotein maturation and impact ER proteostasis, with downstream effects on cell signaling and adhesion. Pathogenic variants in ALG3 are associated with congenital disorders of glycosylation, highlighting its relevance for studying glycosylation-dependent mechanisms in human cell models.
ALG3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ALG3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ALG3. 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 ALG3 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 ALG3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.