PSAT1 Double Nickase Plasmid (h): sc-403001-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PSAT1 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
- PSAT1 Double Nickase Plasmid (h) and PSAT1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PSAT1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PSAT1 Double Nickase Plasmid (h) | sc-403001-NIC | 20 µg | $410.00 | |||
PSAT1 Double Nickase Plasmid (h2) | sc-403001-NIC-2 | 20 µg | $410.00 |
PSAT1 encodes phosphoserine aminotransferase 1, a pyridoxal phosphate–dependent enzyme in the phosphorylated pathway of L-serine biosynthesis that catalyzes conversion of 3-phosphohydroxypyruvate to 3-phosphoserine. Through control of serine and glycine availability, PSAT1 influences one-carbon metabolism, nucleotide synthesis, redox homeostasis, and central carbon flux in proliferating cells. Its activity intersects with amino acid deprivation responses and integrated stress signaling that couple nutrient status to growth and biosynthetic capacity. Altered PSAT1 expression has been linked to metabolic rewiring in cancer and other disorders of amino acid metabolism, supporting its use as a mechanistic node in metabolic and signaling studies.
PSAT1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PSAT1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PSAT1. 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 PSAT1 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 PSAT1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.