L-serine dehydratase Double Nickase Plasmid (h): sc-408194-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- L-serine dehydratase 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
- L-serine dehydratase Double Nickase Plasmid (h) and L-serine dehydratase Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SDS. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
L-serine dehydratase Double Nickase Plasmid (h) | sc-408194-NIC | 20 µg | $410.00 | |||
L-serine dehydratase Double Nickase Plasmid (h2) | sc-408194-NIC-2 | 20 µg | $410.00 |
Human SDS encodes L-serine dehydratase, a pyridoxal phosphate–dependent enzyme that catalyzes the deamination of L-serine to pyruvate and ammonia, linking serine catabolism to central carbon metabolism and cellular nitrogen balance. By modulating the availability of serine-derived one-carbon units and pyruvate supply, SDS activity intersects with amino acid metabolism, redox homeostasis, and bioenergetic pathways. Altered regulation of serine utilization is frequently studied in contexts where metabolic rewiring influences proliferation, stress adaptation, and differentiation programs. Consequently, SDS serves as a useful node for probing how amino acid flux impacts downstream biosynthetic and signaling networks in human cells.
L-serine dehydratase Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SDS locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SDS. 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 SDS 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 SDS-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.